Step 2 CK Notes

HIGH YIELD SHIT

Fever defined as temp > 37.8 or 100 C

Leukocytosis defined as > 11,000 cells

Realize that the best next Management is different that the best next diagnostic step.

1g Proteinuria is pretty bad. 4+ is 3.5 gs.

Aortic Dissection

Aortic dissection presents as SUDDEN, severe chest pain that radiates to the back and causes a widened
mediastinum on CXR. Think of the tearing pain.

Cardiac Tamponade presents with Hypotension, JVD, muffled heart sounds (becks triad), tachycardia,
and pulsus paradoxus (> 10 mmHG drop in systolic blood pressure with inspiration). As blood fills the
pericardial sac, the increased pericardial pressures causes compression of the cardiac chambers, limiting
diastolic filling of the right-sided chambers which then reduces PRELOAD and CO which then causes
Hypotension and Syncope.

Aortic Dissection that presents as SYNCOPE

In Aortic Stenosis which presents with SAD(Syncope Angina, Dyspnea) 1) syncope occurs with ACTIVITY,
2) chest pain or angina is EXERTIONAL and does not radiate to the back. 3) PhyEx would show PULSUS et
Tardus (slow rising and low amplitude pulse). You WOULD not see a widened mediastinum.

Cardiac tachyarrhythmias including atrial and ventricular arrhythmias can cause syncope but they do
not present with SUDDEN chest pain, pulsus paradoxus, or have X-ray signs such as a widened
mediastinum.
Hypovolemia can occur due to acute blood loss or protracted vomiting/diarrhea. These patients would
present with 1) dizziness, 2) postural hypotension (orthostatic where there is > 20 drop in systolic and >
10 in diastolic from sitting to standing), 3) flat neck veins ie NO JVD, and 4) may be in hypovolemic
shock.

Papillary muscle dysfunction is a complication of Acute MI. It causes acute Mitral Regurgitation and
presents with sudden ONSET of 1) pulmonary edema, 2) hypotension, 3) Cardiogenic shock.

Vasovagal syncope would present with 1) Prodromal symptoms including dizziness, nausea, diaphoresis,
pallor, or visual disturbances before the syncope episode.

Pulmonary Auscultation Examination Findings

Principle are:

1) Within the lung, SOUND travels faster through solids and liquids so any process in which this
occurs would have INCREASED Breath SOUNDS and INCREASED TACTILE FREMITUS
2) Outside the lung, Solids and Fluids insulate any sounds from inside the lung and cause
DECREASED breath sounds and DECREASED Tactile Fremitus.

Condition Breath Sounds Tactile Fremitus Percussion Mediastinal Shift

(all about the state
of the LUNG TISSUE
or what surrounds
it)
Normal Normal: Normal Resonant (air) None
bronchovesicular
(hilar), vesicular
(peripheral)
Consolidation Increased Increased Dull (mucous) None
(Lobar PNA) (crackles and (tissue is inflamed
egophony- and denser)
sound travels
faster in
mucous)
Pleural Decreased or Decreased Dull (liquid) Away from effusion if
Effusion absent (hard to (there is fluid around large enough
(fluid outside hear sound the lung, which
lung) through a layer prevents you from
of fluid and cells) vibrating lung tissue)
Pneumothorax Decreased Decreased (there is Hyperresonant Away from a tension PTX
(air outside (insulated by air) air around the lung (lots of air).
lung) which prevents you
from vibrating lung
tissue)
Emphysema Decreased Decreased (there is Hyperressonant None
(extra air (so much air less lung tissue) (more air 2/2 to
inside lung) inside that it is air trapping)
decreased)
Atelectasis Decreased or Decreased Dullness (no air Towards atelectasis if
(collapsed absent (no air) (tight collapsed lung collapsed) large (collapsed lung will
lung or mucus wont shake) pull opposite towards
plugging) itself due to elastic recoil)

Any answer choice where BS and Tactile FREMITUS are not going in the same direction is WRONG.

Metastatic cancer can cause a Pleural effusion.

A pleural effusion would cause BLUNTING of the costophrenic angles.

A consolidation from lobar PNA would not cause blunting of the costophrenic angles.
Tension PTX presents with JVD, hypotension, tracheal deviation seen on CXR.

HIT Type 2 ( Heparin Induced Thrombocytopenia)

Aside: HIT 2 occurs later 4- 10 days. HIT 1 occurs after 2 days and is believed to have a non-immune
mechanism.

Often presents as skin necrosis in the abdominal injection site.

Path: Heparin binding to platelet factor 4 on platelets creates a neoantigen that the body produces
antibodies against. The antibodies attack platelets causing aggregation which then leads to
Thrombocytopenia and PROthrombotic state.

Dx. HIT is diagnosed by 1) Functional assay: Serotonin Release Assay or 2) Immunoassay if they have a
high titer

Tx: Stop all heparin products and start alternate anticoagulant eg argatroban, fondaparinux. If you
suspect hit but results have not come back, still go ahead and stop heparin due to risk of Venous and
arterial thromboses.

WF is an ORAL anticoagulant that can cause acquired protein C deficiency which can also present as
skin necrosis. You can use WF for long-term anticoagulation in patients with HIT.

Delayed hypersensitivity rxns cause skin erythema, vesicles, or bullae. More serious rxn may also cause
fever.

Cholesterol embolization from where a plaque embolizes a small artery presents with skin findings such
as Livedo reticularis (mottled erythema), gangrene, cyanosis, in the LE.

Viral reactivation in a relatively older patient (~60s) points to Herpes Zoster. The lesions are
UNILATERAL, single dermatome, PAINFUL, and vesicular.

Warfarin-Induced Skin Necrosis

Path: WF inhibits production of Vit K factors: 10, 9, 7, 2 and protein CS by blocking regeneration of
Vitamin K. Protein C and factor 7 are the first factors to be lost 2/2 to having shortest half-lives.

Loss of Protein C (anti-coagulant) and remaining presence of 10, 9, 2 creates a hypercoaguable state. So
patients with protein C deficiency are at increased risk for warfarin skin necrosis.

Px: Skin lesions in extremities, breast, trunk, or penis that occurs within first few days of starting WF.
Lesions marginate with a few hours and if untreated become edematous, pruritic, and necrotic.

Tx: Stop warfarin, give Protein C concentrate.

HIT is caused by Heparin binding to platelet factor 4.

Factor 5 Leiden mutation increases the risk of venous thromboembolism: DVTs and PE.

Factor 7 deficiency causes a bleeding with bruising and hemorrhage.

SPECT (Single Photon Emission CT scan) Cardiac stress testing with Technetium-99.

Normal trace uptake at rest and after exercise = Great prognosis < 1% risk of CAD

Decreased trace uptake at rest AND after exercise = Scar tissue (a fixed defect).

Normal trace uptake at rest BUT decreased tracer uptake after exercise indicates inducible ischemia and
CAD. They should be started on an 1) antiplatelet therapy (Aspirin), 2) beta blockers, and 3) life-style
modification (stop smoking, improve lipids, manage diabetes) to reduce risk of future events.

Albuterol can cause tachycardia, elevated BP, and possible arrhythmia so avoid in CAD. Give a Beta
blocker instead.

Appetite suppressants are sympathomimetics (STIMULANTS) so they can increase HR and BP, avoid in
CAD.

Erythropoietin (EPO) should not be given in patients with CAD as it can increase risk of thromboembolic
stroke etc.

Metformin should be avoided in patients with CKD or CVD.

Granulomatosis with Polyangitis (Wegners Granulomatosis)

Px: Upper respiratory: Sinusitis/otitis, saddle nose deformity,

Lower respiratory: multiple Lung nodules/Cavitation, tracheal narrowing or ulceration

Renal: Rapidly progressive GN represented by an Elevated Cr.

Skin: Livedo reticularis, nonhealing ulcers

Demographics: White, Age 30-50.

Dx: Test for C-ANCA, Definitive dx use Biopsy skin to look for leukocytoclastic vasculitis, Kidney for
pauci-immune GN, and Lung for granulomatous vasculitis.

Tx: High dose corticosteroids and cyclophosphamide or Rituximab.

45 y/o man presents with upper respiratory, lower respiratory, elevated Cr, and B symptoms.

Hypersensitivity Pneumonitis caused by a reaction to environmental antigens presents with NON-

caseating granulomas. CXR would show reticular, nodular, or alveolar opacities BUT NOT CAVITATIONS.
Upper airway is less prominent and you would not see any other systems affected.

Squamous Cell lung cancer can cause cavitary lung lesions and B-symptoms but this would be expected
in a patient who is OLDER and HAS a SMOKING HISTORY.

Pulmonary Aspergillosis occurs in IMMUNOSUPPRESSED patients (albuterol inhalers) or structural lung

defects (cystic fibrosis). Only pulmonary symptoms.

Sarcoidosis causes non-caseating granulomas in the lungs and presents with Bilateral Hilar
lymphadenopathy on CXR. It can also involve the kidney but would cause interstitial nephritis (rash,
fever, and eosinophilia) or nephrolithiasis.

Silicosis occurs due to inhalation of silicon dioxide and seen in MINERs and STONE workers. Silicosis
increases the risk of developing active TB which can cause cavitary lung lesion.

In differentiating Crohns from Ulcerative Colitis, the following signs more strongly suggest Crohns

1) Involvement of multiple portions of the GI tract from mouth to anus ( skip lesions)
2) Non-caseating granulomas ( Granny
3) Rectal sparing (ileuming away from the wRECk)
4) Fistula formation (fist)

UC and CD are Initially treated first with 5 aminosalicyclic acids (Sulfasalazine, Mesalamine) and
Corticosteroids. Maintenance therapy is Azathioprine or Anti- TNF factors.

Pulmonary Embolism

Px. Patient with prolonged immobilization (risk factor to develop DVT), presents with 1) SUDDEN-onset
pleuritic chest pain, 2) Dyspnea, 3) Tachycardia. Can also develop small pleural effusions due to
hemorrhage or inflammation which can be painful due to pleural irritation.

Dx. CT pulmonary angiogram, or V/Q scan if they cannot tolerate contrast.

37 yo with MS, wheel-chair bound, presents with SOB, left-sided chest pain, and small pleural effusion for
2 days. Afebrile, normal WBC, no peripheral edema.

Aspirational PNA is common in patients with MS who have bulbar symptoms. It can present with
pleuritic pain and exudative pleural effusion. But you would also see Fever, leukocytosis, cough, and
lobar infiltrate on CXR.
CHF can cause transudative pleural effusions 2/2 to hydrostatic pressure. But the effusions would be
BILATERAL or RIGHT-sided. Would also see signs of volume overload: lower extremity edema, JVD.

Hypoalbuminemia can cause transudative pleural effusions 2/2 to decreased oncotic pressure. The
effusions would be BILATERAL and typically would not present acutely. Would also see ascites, edema.

Malignant effusions are LARGE and present with progressive SOB over several days or weeks (subacute).
Small acute, pleural effusion is more likely PE.

Paroxymal Noctural Hemoglobinuria

Path: RBC and platelets lack GPI anchors CD 55- and CD-59 and so get attacked by complement

Px:

1 Hemolysis: Intravascular hemolysis signs: reduced haptoglobin, elevated LDH, hemoglobinemia,

hemoglobinuria and Extravascular hemolysis signs: elevated unconjugated bilirubin

2 Cytopenias Anemia 2/2 to hemolysis of RBCs: fatigue and dyspnea

3 Hypercoaguable state: Intraabdominal or cerebral vein thrombosis 2/2 to complement attacking

platelets. Common is acute abdominal pain from portal vein thrombosis in Liver.

Demographics: occurs in 40s.

Dx: Flow cytometry test to look for absence of CD 55 and CD 59. Urinalysis to look for hemogloblinuria,
CBC to look for anemia. Measure LDH and haptogloblin in serum.

Tx: Iron and folate supplementation, Eculizumab monoclonal ab that inhibits complement

43 yo woman px with abd pain, RUQ tenderness, and dark urine. Hgb 8.9, hepatic vein thrombosis,
elevated total Bilirubin, elevated LDH, reduced Haptoglobin.

Acute intermittent porphyria can present with abd pain and dark red/brown urine. The pigmented urine
is due to porphyrins and/or porphyrin precursors. They do not develop ANEMIAs or other hematologic
abnormalities or thromboembolism.

Aplastic anemia doesnt present like this.

G6PD can also cause hemolytic anemia but does not cause thrombosis. It is more common in males and
those of African descent. Triggered by medications or infections.

Hereditary spherocytosis does not cause venous thrombosis. More common in Europeans. Would see
increased RDW on CBC and spherocytes on blood smear.

Osteoarthritis (OA)
The major risk factors for OA are 1) Obesity, 2) Age > 50, 3) Prior Joint injury (trauma).

Px Chronic joint pain that is worse after activity and at the END of the day. Minimal/no morning stiffness
ie lasts < 30 minutes. Affects large weight bearing joints: knees/hips, DIP joints, cervical/lumbar spine.

PE: 1) Hard, bony enlargement of joints, 2) small joint effusion without erythema or warmth, 3) Crepitus
and pain with movement and limited ROM,

Dx: 1st line X-ray: show narrowed joint spaces, osteophytes, and subchondral sclerosis, Arthrocentesis
which would show few inflammatory cells; evaluate acute symptoms and rule out septic joint.

Lab studies: ESR, CRP would all be normal.

Tx: NSAIDs, Acetaminophen, and glucocorticoids

65 yo woman with worsening right knee pain for 2 years. Worse at night. Obese at BMI of 34. On exam
has small joint effusion, and bony crepitus. No hx of trauma.

Anserine bursitis occurs in women and obese people. DM increases risk. Presents with localized pain and
tenderness over the ANTERIOMEDIAL tibia distal to joint line. Sx evolve over WEEKS-MONTHS, not
years. Pain is WORSE OVERNIGHT or in Morning. No crepitus or joint effusion.

Iliotibial band syndrome is a common overuse injury characterized by pain at the lateral knee.
Examination shows tenderness at the lateral femoral condyle during flexion and extension.

Lateral collateral ligament (LCL) injury can occur from a blow to the medial aspect of the knee. PE shows
laxity of the knee with VaRus (medial l force with respect to tibia)

Medial meniscus injury occur with twisting movements of the knee and px with crepitus, locking or
catching, and a joint effusion. Presents ACUTELY.

Patellofemoral pain syndrome is an overuse disorder seen in YOUNG women. Px as diffuse ANTERIOR
knee pain that is reproduced by patellofemoral compression during knee extension.

Effects of Hypothyroidism

Hypothyroidism can cause Hyperlipidemia 2/2 to decreasing LDL receptors. Usually patient with will
have either just hypercholesterolemia OR Hypercholesteremia AND hypertriglyceridemia. Rare to have
ISOLATED hypertriglyceridemia.

Hypothyroidism can also cause Hyponatremia and asymptomatic elevation in Cr and transaminases (AST
and ALT).

Hypothyroidism does not affect calcium. Thyroidtoxicosis can cause HYPERCALCEMIA.

Risk factors for Pulmonary Infections

Impaired swallowing and cough reflex increases risk of aspirational pneumonia in dementia patients.
Altered consciousness, dysphagia, GERD, NG or endotracheal tubes, protracted vomiting, and large
volume feeds in bed also increase risk of aspirational PNA.

Impaired mucociliary clearance occurs in smokers and patients with CF or Kartagener syndrome.
Increases risk of pulmonary infections period.

Aspirational PNA

Aspirational PNA typically develops over days and causes low grade fever, dyspnea, and a productive
foul-smelling cough. Location of infiltrate is gravity dependent at time of aspiration. In supine patients:
posterior segment of upper lobes and superior segments of lower lobes.

Tx: Broad spec abx with good Anaerobic coverage: Clindamycin, Amox-Clau etc.

Acute erosive gastropathy

Aspirin decreases protective prostaglandins. Cocaine causes vasoconstriction reducing blood flow to
mucosa (increased risk of injury from acid). Alcohol and aspirin can directly damage mucosa.

Causes of GI Bleeding Hematemesis

33 yo px with abd pain, nausea, vomiting x 2 with small blood in setting of alcohol, cocaine, and NSAID
ingestion.

Aortoenteric fistula CAN present as massive life-threatening GI hemorrhage or mild bleeding. RF are
older age, history of AAA, or cancer.

Esophageal variceal bleeding occurs in patients with Cirrhosis. They would have other findings such as
ascites, spider angiomata, and jaundice.

Pancreatitis presents with SEVERE abdominal pain that radiates to the back and occurs AFTERS YEARS of
heavy alcohol use not a single binge drinking.

Mallory-Weiss tear occurs in the DISTAL esophagus and is 2/2 to repeated bouts of retching and
vomiting. The patient should have a hx of multiple episodes of nausea and vomiting that PRECEDED the
onset of hematemesis.

Esophageal Perforation

Chest pain, Widened mediastinum, SIRS = Boerhave

Causes are
 1) Spontaneous rupture from vomiting or severe straining Boerhave Syndrome
2) Instrumentation from Endoscopy
3) Esophagitis (infectious, pill, caustic)
4) Esophageal ulcer that ruptured.

Px:

1 Chest, (retrosternal) and abdominal pain + systemic findings: Fever, hypotension, Tachycardia,
Tachypnea etc 2/2 to gastric leak with tons of bacteria into mediastinal space.

2 Subcutaneous emphysema in neck aka crepitus

3 Odynophagia pain with eating

4 Hamman sign crunching sound on chest auscultation

Dx

CXR or CT scan showing widened mediastinum, PTX, air around paraspinal muscles,

Unilateral EXUDATIVE Pleural effusion, usually LEFT, that is high in AMYLASE, low PH. May also contain
food particles.

CT scan shows esophageal wall thickening, mediastinal air fluid level.

Water-soluble contrast esophagogram will leak at perf site.

Tx: Make NPO, Give IV PPI and Abx + IV fluids/nutrition (supportive). Surgical repair: drainage
debridement, or closure for significant leakage with SIRS.

41 yo px with SUDDEN retrosternal and abd pain after vomiting for last several hours. Hx of alcohol
use. Febrile, hypotensive, tachycardic, palpable crepitus, tender in epigastrium

Acute MI presents with chest pain but remember that it is NON-tender, Non-positional, and Non-
pleuritic. Should NOT have crepitus or be febrile.

Acute pancreatitis presents with epigastric pain that radiates to the back (in contrast to Aortic dissection
is tearing chest pain that radiates to the back).

A perforated duodenal ulcer would cause epigastric pain with FREE AIR under the diaphragm on CXR.
You would not SEE crepitus (pneumomediastinum).

Mallory-weiss tear presents with hematemesis BUT NOT pneumomediastinum.

Rupture of bullae can cause spontaneous PTX (in tall, skinny male) but would not be febrile and would
have more lung findings eg diminished lung sounds etc.

32 yo, midline chest pain for 4 hours, px with hypotensive, slight fever, tachycardic. CXR shows widened
mediastinum and left-sided pleural effusion high in amylase.
Acute pancreatitis would present with a pleural effusion high in amylase but would not see widened
mediastinum

Aortic dissection can also present with chest pain, hypotensive, tachycardic, and even pleural effusion
(hemothorax) but you would not see HIGH amylase level.

Urinary Tract Infections

Staghorn calculi increase the risk of UTIs Patients px with irritative urinary symptoms, flank pain, and
hematuria

Emphysematous pyelonephritis occurs in patients with diabetes. Presents fever, chills, flank or abd pain,
and nausea/vomiting.

Bladder cancer presents with irritative urinary symptoms and painless hematuria.

Treatment of DVTs

A patient presents with a DVT.

1) If they are found to have a concurrent PE or have a Massive DVT with severe swelling or life-
threatening ischemia

Look at Thrombolytics.

If there are no contraindications give tPA. If this fails then surgical approach.

IF there are contraindications to thrombolytics go for a surgical approach: mechanical

thrombectomy, iliac stenting, or surgical thrombectomy

2) If they just have a DVT (mild to moderate)

Look at Anticoagulation
o IF there are no contraindications to AC such as significant Active bleeding, recent
surgery, acute hemorrhagic stroke etc Use AC such as hep/WF bridge. For WF INR
needs to be b/w 2-3.
o IF there are contraindications to being on AC or if AC failed meaning the patient
developed a new DVT while on a drug, then place an IVC filter.

Compression stockings are used to treat post-thrombotic syndrome where the patient can have pain
swelling and venous ulcers from chronic venous insufficiency after a DVT. They are not used to prevent
DVT.

In a patient with COPD indicating they already have low lung reserves, you def want to treat large
proximal DVTs.
Lymphadenopathy and Splenomegaly in an old man points to Lymphoma or Leukemia. Anemia results
from infiltration and crowding out of RBC progenitor cells by Cancer cells in the bone marrow.

Intravascular hemolysis causes include 1) prosthetic valves, DIC, TTP, HUS, and PNH.

Autoimmune hemolytic anemia that occurs in patients with CLL is Extravascular as it occurs in the spleen
and reticuloendothelial system.

For aplastic anemia, you would NOT SEE SPLENOMEGALY.

Malignant Necrotizing Otitis Externa (MOE)

Severe infection of the external auditory canal and base of skull caused by Pseudomonas Aeruginosa.

Px. Patients are usually older and have poorly controlled diabetes or immunosuppressed. Severe
unrelenting ear pain, worse at night, with purulent drainage and a sense of fullness and conductive
hearing loss. Pain can be exacerbated by chewing if osteomyelitis of the skull base occurs.

Dx Otoscopy shows granulation tissue and edematous external auditory canal.

Tx: 1st line is IV Cipro. If fluoroquinolone resistant, then anti-pseudomonal penicillins or cephalosporins
such as Piperacillin, Ceftazidime. Surgical debridement is NOT needed.

78 yo woman hx of DM presents with severe left ear pain worse at night, with discharge, exacerbation
with chewing. Granulation tissue seen on otoscopy.

Cholesteatoma is a keratinized epithelial growth in middle ear which can present with hearing loss and
discharge but would not see SEVERE ear pain, fever, and elevated ESR. This is treated surgically.

Topical abx and steroids are used for Otitis externa. Difference b/w OE and MOE is severity of the pain,
presence of granulation tissue, and elevated ESR in MOE indicating that its bad.

Pneumothorax (PTX)

PEEP can cause a PTX. PTX presents as unilateral absent breath sounds on affected side, impaired
ventricular filling which presents as hypotension, tachycardia. As the intrapleural space fills with air and
compresses nearby structures, it impinges on the central veins, which then increases central venous
pressure aka JVD. You would also see tracheal deviation away from the affected side on CXR.
Cardiac tamponade presents with hypotension, tachycardia, and elevated central venous pressure aka
JVD. But it would cause muffled heart sounds and not affect lung sounds.

Endotracheal intubation of the right mainstem-bronchus can cause atelectasis of the left lung. This
would present as cough, dyspnea, and decreased oxygen saturation. You would see no cardiac effects
so no hypotension, tachycardia etc.

PE presents with sudden onset SOB, tachypnea, hypoxia, and potentially hypotension. But you would still
hear lungs sound as it does not affect lung sounds (air can still flow in the lungs).

Obstructive Sleep Apnea

Px Obese, middle age person who presents with daytime sleepiness, early morning headaches,
increased fatigability, and loud snoring. May also have HTN.

Dx Polysomnography

Tx. 1st line Weight reduction, avoidance of sedatives and alcohol, avoidance of supine posture during
sleep.

2nd line for more severe cases: CPAP, and Uvulopalatopharyngoplasty

Autosomal dominant Polycystic Kidney Disease

Px:

Renal Symptoms: HTN, Hematuria, Proteinuria, Palpable renal masses, and Progressive renal
Insufficiency. May also have flank pain 2/2 to renal calculi, cyst rupture or hemorrhage or upper UTIs.

- HTN is a common early finding in patients with ADPKD and occurs before any real kidney
dysfunction occurs.

Extra-renal symptoms are: Cerebral aneurysms, hepatic or pancreatic cysts, cardiac valve abnormalities
(MVP or AR), colonic diverticula, and ventral or inguinal hernias.

Dx: Abdominal Ultrasound or CT showing enlarged kidneys with numerous cysts.

Tx: ACE-Is to control HTN. ESRD- dialysis or renal transplant.

36 yo man px with BP of 175/103 and c/o of occasional morning headaches. Father died suddenly at
age 54. PE shows bilateral, nontender, upper abdominal masses.
Cushing syndrome is diagnosed with 24 hour urine cortisol excretion. Px is central obesity, facial
plethora(red face), proximal muscle weakness, abdominal striae/ecchymosis. Tumors are rarely
palpable.

Renal artery stenosis can be diagnosed with Captopril radionuclide renal scan. No palpable kidney

Primary aldosteronism is dx with a high plasma aldosterone/renin ratio. Patients present with resistant
HTN or HTN with unexplained Hypokalemia. No palpable kidney.

Pheochromocytoma can be dx with increased urinary excretion of vanillylmandelic acid and

metanephrines. Px with pounding headaches, palpitation, and diaphoresis associated with paroxysmal
elevation in blood pressures ie should be EPISODIC. You would not be able to palpate the adrenal
glands.

Chronic Primary Adrenal Insufficiency aka Addison Disease

Path: Autoimmune (most common) Infections eg TB, HIV, fungal, Hemorrhagic infarction (waterhouse
friedrickson), and Metastatic.

Px

Initial symptoms are nonspecific things such as fatigue, malaise, weakness, weight loss, syncope.

GI symptoms n/v, abd pain, diarrhea, hypoglycemia are common.

Aldosterone deficiency causes volume depletion, hyponatremia, hyperkalemia (NO aldo to reabsorb Na
means K+ is not excreted) hypotension, postural dizziness, or syncope

Skin signs are generalized or patchy HYPERPIGMENTATION 2/2 MSH which is secreted with ACTH or
Vitiligo 2/2 to auto-immune destruction of melanocytes.

Volume depletion leads to increased ADH which results in a dilutional hyponatremia and mild
hyperchloremic acidosis.

Dx. Measure ACTH, serum cortisol level or high dose (250 ug ACTH stimulation test)

Primary: low cortisol and high ACTH

Secondary/Tertiary: low cortisol, low ACTH

Infectious Genital Ulcers

PAINLESS Ulcers

1 Syphillis is Painliss, and is SINGLE ulcer with regular borders and hard base.

LGV from chalmydia is also PainLess and presents with MULTIPLE, small shallow ulcers that can progress
to painful buboes aka fluctuant adenitis.
PAINFUL Ulcers

Hemophilus Ducreyi presents as a 1 or more PAINFUL papules that become large deep ulcers with
gray/yellow exudate and well demarcated borders with a soft friable base and SEVERE inguinal
lymphadenopathy. With Ducrey you Du-Cry (PAINFUL) More common in developing countries rare in
US but outbreaks in peeps who trade sex for money and drugs.

HSV presents as PAINFUL, MULTIPLE small vesicles or ulcers on an erythematous base. May have some
mild lymphadenopathy.

Acute HIV presents with mono-like symptoms: fever, fatigue, sore throat, painless lymphadenopathy,
generalized rash, and painful mucocutaneous ulcerations with a shallow, sharply demarcated and a
white base.

Neisseria Gonorrhoeae causes cervicitis or urethritis, it does NOT cause genital ulcer.

1 syphillis presents with a painless papule that converts into an ulcer with raised, indurated margins and
a non-exudative base.

Staphylococcal Ecythma is a deep form of IMPETIGO that begins as a vesicle/pustule on an inflamed area
of skin and becomes an indurated purulent ulcer. Lesions are common on the buttocks, thighs, and legs.

Elevated Enzyme Ratios

Patients with an UPPER GI bleed often have an elevated BUN/Creatinine ratio 2/2 to increased intestinal
breakdown of hemogloblin which is then converted to Urea and reabsorbed (globin is protein so it
contains nitrogen). Also, bleeding causes hypovolemia which would increase reabsorption of Urea in
kidneys.

Aldosterone/Renin ratio is elevated in 1 hyperaldosteronism (CONN syndrome) 2/2 to uncontrolled

aldosterone release which then suppresses RENIN.

Alkaline phosphatase (Alk Phos) is elevated in biliary obstruction, and bone disease where there is
increased OSTEOBLAST activity eg. Pagets disease.

Prolonged PT can be seen in patients with WF, Vitamin K deficiency, liver disease, abx use (kill all the
bacteria that produce Vit K), and hereditary coagulation disorders.

Prolonged PT can be seen in warfarin use, Vitamin K def, Liver disease, and Abx use.

FENA is low in patients who are volume depleted as it the kidneys attempt to retain sodium to restore
blood volume. FENa is HIGH in intrinsic renal disease.

Gout

Px: sudden onset SEVERE pain in the first metatarsophalangeal joint (podagral).

Tx:

Acute Attack: 1st line NSAIDs eg Indomethacin or Glucocorticoids 2nd Line Colchine
Chronic Attacks: For patients with recurrent attacks or severe disease represent by presence of Tophi,
uric acid kidney stones etc: Use urate-lowering therapy: 1st Allopurinol/Febuoxstat 2nd Pegloticase

Lifestyle Modifications:

1. LOSE WEIGHT and restrict calories; aim for BMI< 25

2. Stop eating Red meat and seafood and pick up Vegetarian and low-fat diet
3. Stop drinking sugary beverages (contain fructose and other refined sugars) and Alcohol as
ethanol increases uric acid production while decreased excretion
4. Consumption of coffee (not tea) lowers uric acid and reduces risk of gout
5. Smoking also lowers risk of GOUT attack.

Pellagra (Niacin or NAD or Vitamin B3 deficiency)

Path: Causes

1) Dietary deficiency seen in developing countries in patients who mainly eat corn products; in
developed countries seen in alcoholics and those with chronic illness
2) Carcinoid syndrome Tryptophan is shunted into making Serotonin so none left to make
Vitamin B3
3) Prolonged Isoniazid therapy Vitamin B6 is needed to make NAD. No B6 then no B3.
4) Hartnup disease AR where unable to absorb tryptophan (congenital disorder)

Px 3 Ds

1. Dermatitis rough, dry, hyperpigmented scaly skin on SUN-EXPOSED areas of the body
2. Diarrhea- often associated with Abd pain, nausea, and loss of appetite
3. Dementia 2/2 to neuronal degeneration. Can cause memory loss or affective symptoms: eg
depression and psychosis

42 y/o from northern Africa, mainly east corn, on isoniazid and pyridoxine for latent TB, presents with
abd pain, watery diarrhea, skin rash that worsens with skin exposed, and feels depressed.

Acute intermittent porphyria (AIP) causes abd pain, vomiting, and diarrhea with NEUROLOGIC symptoms
and Psychiatric symptoms such as agitation, confusion, depression and paresthesias from
polyneuropathy. You would also see dark urine and urinary problems.

Isoniazid hypersensitivity is when a patient develops hive maculopapular rash with pruritus, fever, and
hepatitis from INH. A scaly rash is not a hypersensitivity rash.

Seborrheic Dermatitis presents with erythematous, scaly plaques that affect the scalp, face, chest, and
intertriginous areas. It can be associated with dementia but typically does not cause any GI symptoms
and spares the hands.

SLE causes a photosensitive rash in a malar distribution (butterfly pattern). Can have CNS symptoms
such as psychosis. Isoniazid can cause drug-induced Lupus but the rash is less common.
Ethics Question: Breaking bad news

When breaking bad news always have a patient centered approach eg. First step is to figure out what
the patients understanding of the disease is. Try to avoid overloading the patient with too much
information.

Use the SPIKE mnemonic: Set the stage, Perception what is your understanding Invitation: how do u
like your medical information, what do you want to know? Knowledge, Empathy

Carpal Tunnel syndrome is usually diagnosed clinically but you would use a Nerve Conduction Study to
confirm.

Electromyography measures the electrical activity of muscles can be used in prep for surgery for CTs.

MRI of the cervical spine is indicated in patients with cervical radiculopathy: neck and upper arm pain,
diminished reflexes or Cervical spondylotic myelopathy: bilateral UMN signs and bilateral sensory
deficits.

Workup of patient who presents with Hyperbilirubinemia

A patient presents jaundice and dark urine.

If the bilirubin is MOSTLY conjugated bilirubin then the problem lies either in the Liver or in the CBD.

Next step: Look at the liver enzyme pattern

1. Predominant AST and ALT: Viral hepatitis, Autoimmune hepatitis, Toxin/drugs,

Hemochromatosis, ischemic hepatitis, alcoholic hepatitis eg something that damages the
Liver directly (hepatic dysfunction) Patients have a positive Urine urobilinogen and bilirubin
assays.
2. Normal AST, ALT, and Alk Phos: Dubin: Johnsons Syndrome or Rotors Syndrome. Eg defect
in hepatic bilirubin secretion. Patients have a positive urine bilirubin assay but negative
urobilinogen assay.
a. Rotors Syndrome: a rare benign hereditary condition with chronic of fluctuating
conjugated hyperbilirubinemia that is DUE to a defect in HEPATIC secretion of
conjugated bilirubin into the biliary system. Usually discovered in childhood;
TREATMENT IS UNNECESSARY.
b. Dubin-Johnson similarly, isolated increase of conjugated bilirubin in the blood.
Causes a BLACK liver. Also, asymptomatic; no treatment needed.
3. Predominantly Alk Phos: Cholestasis of pregnancy, Malignancy (pancreatic or ampullary),
Cholangiocarcinoma, Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis, and
Choledocholithiasis. Eg something that is blocking the CBD (biliary obstruction)
a. If you suspect blockage your next step is Abd ultrasound or Abd CT and
Antimitochondrial antibody.
If the bilirubin is MOSTLY unconjugated bilirubin then the problem is in production either

1) Overproduction from hemolysis:

a. Patient would have a positive urine Urobilinogen assay but negative urine bilirubin
assay as there is excess Unconjugated bilirubin which is not soluble.
2) Reduced uptake from drugs/portosystemic shunt,
3) Conjugation defect as seen in GILBERTs Syndrome.

For Choledocholithasis or Cholangitis, ERCP is performed after the initial U/S or CT scan to show that
there is actually blockage the in CBD.

Bilirubin metabolism

Heme Unconjugated bilirubin (Liver UDP glucuronyosyl) Conjugated bilirubin some conjugated
bilirubin enters the blood/ MOST conjugated bilirubin secreted in to duodenum Urobilinogen
Some/reabsorbed in the blood and enter urine/Some remain intestines and converted to Stercobilin.

Positive Urine Bilirubin assay detects Conjugated bilirubin in the urine and indicates there is a BUILDUP
of conjugated bilirubin in the blood.

Positive Urine Urobilinogen assay detects Urobilinogen and tells you excess Urobilinogen is being made,
indicating there is OVERPRODUCTION.

Hemodynamic Measurements in Shock

Parameter Normal Hypovolemic Cardiogenic Shock Septic Shock/

Shock = Pump Failure Distributive
Shock/
Vasodilatory
Shock/
= Massive dilation
of vessels
RA pressure ~4 mm Hg Decreased Increased (blood Normal to
is backed up in decreased
veins)
PCWP (pulmonary ~ 9 mm Hg Decreased Increased (heart is Normal to
capillary wedge stuck so blood decreased
pressure) remains backed
up in veins)
Cardiac Index 2.8-4.2 L/min Decreased Severely Increased (heart
(pump function) Decreased now has to work
harder to
 maintain BP since
SVR has dropped
SVR (afterload) 1150 dyne Increased (you Increased (heart Decreased
have low BP so not pumping, BP
body wants to decreases so body
maintain BP by tries to maintain
constricting BP by constricting
vessels) vessels)
MvO2 (mixed 60-80% Decreased (more Decreased (more Increased
venous oxygen O2 is being O2 is being
saturation) extracted from extracted from
the little blood so the little blood so
saturation should saturation should
decrease) decrease)

In hypovolemic shock, loss of intravascular volume decreases left ventricular preload which decreases
CO and blood pressure. This then causes sympathetic stimulation to compensate which increases HR
and peripheral vasoconstriction to try to maintain CO.

Septic shock aka distributive shock from anaphylaxis, SIRS, or CNS injury is caused by low SVR and BP.
Leads to compensatory increase in HR and CO.

An elevated SVR with a normal BP, CO, and PCWP is consistent with PRE-SHOCK or Compensate shock.
This is when the patient experiences a small decrease in CO and BP but this is compensated by an
increase in SVR and HR. This allows for maintenance or a normal CO and BP and perfusion for a while.
But as the underlying condition worsens, the heart rate cannot sustain adequate CO and shock occurs.

Elevated BP, CO, and SVR with a normal PCWP suggests a Hyperadrenergic state (lots of epi and norepi)
due to a catecholamine surge or PRE-ECLAMPSIA. Hyperreflexia is a sign of pre-eclampsia.

Iron Overload

Px: Late causes skin pigmentation, diabetes, heart failure, and cirrhosis.
Vitamin B12 deficiency (Cobalamin)

Path:

Vegetarians are at risk for developing Vitamin B12 def. especially if dairy consumption is low, Vegans are
at an even higher risk they dont eat dairy.

Alcoholic and Vegetarian means the patient would be deficient in FOLATE (alcohol) and Vitamin B12
(vegetarian) which can both cause megaloblastic anemia.

Chronic gastritis or Gastrectomy could cause a VB12 deficiency by decreasing production of intrinsic
factor (pernicious anemia).

Chronic malabsorption from a condition like Crohns disease, ileal resection/damage, fish tapeworm
(diphylobothrium latum) could cause B12 def.

Px. Vitamin B12 deficiency causes Sub-acute Combined Degeneration and Megaloblastic anemia

S- Spinocerebellar tract = Ataxia

Corticospinal tract = weakness of muscles, UMN signs

D-Dorsal column = loss of proprioception, numbness/paresthesias

D- Dementia = depression, dementia, memory deficits etc

Labs: Macrocytic anemia (MCV > 100), Increased homocysteine and Methylmalonic acid (folic acid has
increased homocysteine but normal methylmalonic acid)

Peripheral blood smear shows Macro- cytic RBCs and hypersegmented Neutrophils (> 6 bends in
nucleus)

Tx. Replenish B12;

giving folate w/o B12 may fix megaloblastic anemia but will cause RAPID progression of neurologic
symptoms.

45 yo man px with fatigability, he is vegetarian and alcoholic, Hgb 10.8. Given thiamine and folate but
returns 3 months later because of falls and forgetfulness.

32 yo Crohn disease, present with LE paresthesias and difficulty with balance, UMN signs.

D-lactic acidosis occurs in patients with short bowel syndrome. Unabsorbed carbs are converted to d-
lactic acid by bacteria which is absorbed and then causes acidosis. Pt usually are asymptomatic but can
develop episodes of confusion, ataxia, and dysarthria after eating a lot of carbs.

MGUS and MM can present with polyneuropathy and a NORMOCYTIC anemia.

Hypothyroidism can cause MACROCYTIC anemia and polyneuropathy but on PE you would see a
decrease in DTR.
Internuclear Ophthalmoplegia occurs in Multiple Sclerosis and Cerebrovascular disease where MLF is
involved.

Late neurosyphillis causes tabes dorsalis, lancinating pains, sensory ataxia, and argyle robinson pupils
(most common feature). FTA-ABS is the confirmatory test for syphilis.

Iron deficiency

Path: Elderly patient

Use of NSAIDS and aspirin can cause gastrisitis/gastric ulcers which can lead to chronic blood loss.

Px: symptoms of anemia: fatigue, pallor of mucosa etc

PICA: appetite for non-food items: paper, clay, dirt, ice (very specific for Fe-deficiency)

Kolionychia (spoon-shaped nails)

Oral leukoplakia is a precancerous white patch or plaque on oral mucosa that has 1-20% chance of
progressing to cancer in 10 years.

80 yo man, px with fatigue and conjunctival pallor. Hx of osteoarthritis, uses NSAID + Aspirin

Anemia of chronic disease occurs with Rheumatoid arthrthis and lupus but not osteoarthritis.

Hypothyroidism can cause a mild anemia.

Asthma

Px

With an asthma exacerbation, the patient should have an increased respiratory drive and be
hyperventilating making PaCO2 lower than normal.

Leukocytes can be elevated because of stress.

Tx
For mild to moderate asthma, give O2 and SABA. If they dont respond add systemic glucocorticoid (oral
or IV)

For severe asthma, give SABA + Ipratropium and Systemic glucocorticoid. If no improvement, can give
Epi (inhaled = sub Q), and then one time dose of IV Mag sulfate.

Do NOT USE IV abx or methylxanthines for acute asthma exacerbation.

With severe asthma exacerbation, signs of impending respiratory failure are

1) ELEVATED or NORMAL PaCO2 which means their respiratory muscles are tiring out.
2) Decreased breath sounds
3) No wheezing or faint wheezes
4) Marked hypoxia with cyanosis

When you see these signs, need to INTUBATE the patient.

Methylxanthines, Inahled Cromolyn (mast cell stabilizer), and Zafirlukast (LTD4 leukotriene-receptor
antagonist) are used for management of Asthma. They are not used for acute exacerbations or to treat
COPD.

COPD

Path: Hx of smoking; exacerbation is most commonly triggered by an URI.

Px: Change (increased) SOB, increased (more frequent or severe) cough, and change in sputum
production (change in color or volume).

Dx: CXR to look for Hyperinflation

ABG: Hypoxia, CO2 retention

Tx

Oxygen w/ target of 88- 92%

Inhaled bronchodilators: eg dueo-nebs so beta 2 agonist + ipratropium

Systemic glucocorticoids eg IV or Oral Methylpredinisolone - decrease risk of relapse, treatment failure,

and reduce length of hospital stay.

Abx if they have 2 or more cardinal symptoms

Oseltamivir if they have flu-symptoms

NPPV (Noninvasive Positive Pressure Ventilation) if they are in respiratory failure; failure to respond to
NPPV or contraindicated, Intubate
Methylxanthines, Inahled Cromolyn (mast cell stabilizer), and Zafirlukast (LTD4 leukotriene-receptor
antagonist) are used for management of Asthma. They are not used for acute exacerbations or to treat
COPD.

Cardiac Rhythm Defects

Approach to wide-complex Tachycardia

A patients EKG shows WIDE QRS complex and Tachycardia.

1) If there is Atrial and Ventricular dissociation (p waves separate form QRS) or Fusion/Capture
beats?
a. If Yes, then this V-Tach.
i. If the patient is stable treat with IV Amiodarone; no improvement can try
lidocaine, sotalol, procainamide
ii. If the patient is unstable: hypotensive, AMS, or in respiratory distress, acute
heart failure, pulmonary edema, ischemic chest pain, then synchronized
Cardiovert them
iii. If the patient has Ventricular Fibrillation or pulseless Ventricular Tach, then
treat with immediate defibrillation (unsynchronized shock).

2) IF there is no AV dissociation or a Fused beat.

a. Then this is SupraVentricular Tachycardia (SVT)
i. If the patient is stable, treat with maneuvers to determine rhythm: carotid sinus
massage, rate control
ii. If the patient is UNSTABLE: Hypotension, AMS, resp distress, then synchronized
Cardiovert

Paroxysmal Supraventricular Tachycardia (PSVT) is a regular, narrow complex tachycardia.

Path: is re-entry into the AV node

Px: HR in 160s 220s

Tx. Decrease AV nodal conduction.

1. Vagal maneuvers: valsava, carotid sinus massage, emersion into cold water
2. Adenosine
Digoxin is used to treat Atrial arrhythmias such as A flutter, A fib, and A tachycardia by directly
stimulating the vagus nerve.

Causes of Death in Patients

In dialysis patients, Cardiovascular disease is still the MOST common cause of death (50%). Of the 50%,
20% from acute MI and 60% from sudden cardiac death.

MOA: is dialysis patients have hyperphosphatemia and increased PTH which leads to more
calcium, Ca2+ accelerates atherosclerosis.

CVD is also the most common cause of death in Renal Transplant patients.

Hyperosmolar Hyperglycemia Nonketotic Syndrome (HHNS)

Path: Relative insulin deficiency that causes a state of profound hyperglycemia-induced dehydration
high serum osmolarity classically seen in elderly type 2 diabetics.

Px:

Elderly patient with T2DM

Hyperglycemic symptoms: thirst (polydipsia), polyuria, lethargy, AMS

Lab values:

Glucose > 1000,

Serum Osmolarity > 320 mOsm/kg (285 ~ is normal)

Normal pH and Bicarb, Normal Anion gap, Negative or small serum ketones

Tx

1 Aggressive hydration with normal saline the MOST important initial step

2 IV insulin (regular or short acting insulin)

3 Careful monitoring and supplementation of Potassium

- Despite having normal-elevated K, they have a total body K deficit.

o Increased osmolarity in blood draws K+ out of cells into blood
o Diuresis increased Na+ delivery to distal tubules which increases excretion of K+

Retroperitoneal Hematoma

Risk factors: Diabetes, Older than 60, HTN, alcoholism, and being on anticoagulation.
Px Back pain and signs of internal hemorrhage: fatigue, anemia, tachycardia

Dx Abdominal CT

A 70 y/o patient on anticoagulation, presents with signs of internal hemorrhage: weakness and
dizziness, and evidence of anemia, and tachycardia AND complains of back pain. This should make you
think of Retroperitoneal Hematoma.

Renal cell carcinoma presents with the triad of hematuria, abdominal mass, and flank pain. On abd CT
you would see a mass in the kidney that enhances with contrast.

Vertebra fracture would cause back pain and can occur without trauma but is less likely to cause
bleeding.

Hydronephrosis: dilation of the renal pelvis from obstruction of the genitourinary system. It would
present with flank pain and CT scan would show dilation of the renal pelvis.

Mesenteric Ischemia presents abd pain that is out of proportion to the physical exam findings. It is
common in elderly patients and due to ischemia of the small bowel from a cardiac embolus or arterial
thrombosis. CT findings show bowel wall thickening, pneumatosis intestinalis: gas in the wall of the
intestines, and mesenteric thrombi. Differentiate from Ischemic colitis which is non-occlusive and is due
to reduced blood flow (hypovolemia)

Drug-Induced Acne

Path: Patient recently starts Glucocorticoids: systemic, oral, or topical., Androgens, Azathioprine,
Cyclosporine, Anticonvulsants, Anti-TB drugs

Px. Monomorphic papules or pustules in same stage of development, without comedones that appear
on the upper back, shoulders, and upper arms think of a steroid user with bumps on his upper back

Tx. Stop offending medication; acne meds will not help

28 yo with Lupus recently started oral predinisone and develops uniform pimples on upper back. Works
in a dry-cleaning facility and is sexually active.

Acne vulgaris: pimples in VARIOUS stages of development, usually on the face. Usually in ADOLESCENTS

Chloracne is a severe skin disorder caused by exposure to halogenated hydrocarbons. Defined as

INFLAMMATORY nodules with large comedones affecting head, neck, and axillae.

Lupus usually presents with a MALAR rash in butterfly pattern on face, discoid plaques and ulcers, and
generalized skin photosensitivity

Disseminated Gonococcal infection- presents with a vesiculopustular rash in the distal extremities
(hands and feet) WITH tenosynovitis, migratory polyarthragias, and fever.
Herpes Simplex Virus presents with clusters or vesicles and ulcers on an erythematous base in the
perioral or genital areas.

PREVENTATIVE SCREENING

Influenza

Flu vaccine is recommended yearly for all patients > 6 months and should be given in the fall.

Diabetes Screening

If a patient has a sustained elevated BP (>135/80), if they are older than 45, or if they have risk factors
for diabetes such as HTN, obesity and family history.

Screening tests are 1) fasting plasma glucose (> 99 is positive) 2) 2 hour oral glucose tolerance test
(OGTT) (180, 155, 14) 3) HbAc1

Lung Cancer Screening

Lung cancer screening is indicated in adults 55 - 80 with a 30 or more pack per year smoking history and
who are still smoking or stopped smoking with 15 years. Screen with low-dose chest CT.

Gynecologic/ PAP smears

HPV vaccine is only indicated for Males and Females age 9 - 26.

Begin pap smear testing at age 21 regardless of age of coitarche

Pap tests are done every 3 years from age 21-20. Once over 30 can choose 3 years(PAP only) or 5 years
(PAP + HPV DNA testing. Can stop testing at age 65?

Woman with HIV should get a PAP twice for the first year, and every year afterward

Pneumococcal Vaccination

13 valent pneumococcal conjugate vaccine (PCV13) is recommened for all adults age 65 or older and is
followed by a 23 valent (PPSV23) 6-12 months later. Pneumococal looks like 65.

Sequential PCV13 and PPSV23 Pneumococcal vaccine is also recommended for adults younger than 65
with HIGH-risk underlying conditions eg CSF leaks, sickle cell disease, asplenia, immunocompromised,
chronic kidney failure

PPSV23 alone is recommended for adults age < 65 who are current smokers or have heart or lung
disease, diabetes, and chronic liver disease. if youre sicker you need that BIG 23 dose early.
Chronic Liver Disease Patient who is not vaccinated for Hep A and Hep B should be vaccinated
(especially important) since you do not want further inpyosult to their liver function.

Tdap Vaccination

Single dose of TdAP vaccine at age 11-18 and repeat every 10 years. Td every 10 years. As an adult,
you should get Tdap in place one dose of Td.

A dose of TdAP is recommended for each pregnancy regardless of the last time she had a TdAP.

If a patient has not received Tdap as an Adult or vaccine hx is unknown give Tdap. Then continue by
giving Td booster every 10 years.

Colorectal Cancer Screening

Starting at age 50 patients can begin screening for colorectal cancer by

1. Colonoscopy every 10 years

2. Flexible sigmoidoscopy every 5 years AND FOBT every 3 years
3. FOBT every year

In patients with a family hx of colorectal cancer, screening starts 10 years before the age of dx of a first
degree relative or at age 40. Whichever comes first.

Herpes Zoster

Recommneded in adults > 60.

Skin Conditions and Associated Diseases

Benign Acanthosis Nigricans in a younger/obese individual points to an Insulin-resistant state eg

diabetes, obesity, PCOS

Malignant Acanthosis Nigricans in a middle-aged/elderly patient that is not obese, and appears suddenly
points to an underlying malignancy.

Explosive onset of multiple seborrheic keratosis points to GI malignancy.

Dermatitis herpetiformis = Celiac Disease

Sudden onset severe psoriasis, Recurrent herpes zoster, or disseminated molluscum contagious points
to HIV

Severe seborrheic dermatitis points to HIV or Parkinson Disease.

Pyoderma gangrenosum points to IBD.

Palpable purpura or Porphyria cutanea tarda point to Hep C.

Acanthosis Nigricans pigmentation is described hyperkeratotic, hyperpigmented plaques with a VELVETY

texture. Flexural areas including axilla, groin, and posterior neck are the most common locations
affected.

Hypergimentation in Addisons disease is generalized and is more prominent in areas exposed to

friction. You would also see vitiligo.

Hemochromatosis causes a brownish/bronze or slate gray pigmentation and is more prominent in sun
exposed areas such as the face.

Niacin def aka pellagra presents with photosensitive dermatitis, diarrhea, and dementia.

Urethritis in men

Path: caused by Neisseria gonorrhoaeae (MOST common), chlamydia, Mycoplasma genitalium, and
Trichomonas (rare) in a male who is sexually active.

Px: Dysuria, discharge, urgency, and increased frequency

Dx: Urinalysis, Gram stain and culture, NAAT of first catch urine sample

Tx: Azithro or Doxy + Ceftriaxone if Gonorrhea is not ruled out

A swab described as no GROWTH on gram stain and culture negative is likely Chlamydia.

Gonorrhea is described as Gram negative intracellular dipolococci

Lights P Criteria for Effusions

L- LDH if pleural LDH is > 0.6 serum LDH or is > 2/3 ULN = Exudate

Protein if pleural protein is > 0.5 serum protein = Exudate

Exudative effusions are commonly caused by 1) Infections aka parapneumonic effusion: TB, fungal,
empyema 2/2 to increased capillary permeability from inflammation 2) Malignancy 3) Pulmonary
Embolism, 4) Chylothorax: block of the thoracic duct.

Signs of an infection include pleuritic pain, lymphocytosis in pleural fluid and fever.

Transudative effusions are caused by 1) Hypoalbuminemia from cirrhosis or nephrotic syndrome 2/2 to
decreased plasma oncotic pressure 2) CHF 2/2 to increased hydrostatic pressure and 3) Atelectasis 2/2
to decreased intrapleural pressure.

Chylothorax results from malignancy or trauma that blocks the thoracic duct. It is an EXUDATIVE
effusion that is high in Cholesterol content and is milky white in appearance. There is no inflammation
involved.

Drug Side Effects

Trimethoprim can cause Hyperkalemia by blocking E-Nac transporters in the collecting tubule similar to
amiloride and triamterene and can falsey increase serum Creatinine by blocking renal secretion of Cr
though GFR is not affected.

Macrolide Abx can cause prolonged QT and cholestasis.

Ceftriaxone can also cause cholestasis.

Hemochromatosis

Path- Increased total body iron deposits in multi-organs and causes multisystem organ failure.

Px. Patients present in 30s-50s; with woman presenting later due to losing Fe from menses.

Initially patients will have elevated liver enzymes with hepatomegaly and high ferritin/serum iron but as
iron accumulates develop other symptoms.

Skin Hyperpigmentaion with brown/bronze skin

MSK Arthralgia, arthropathy, chondrocalcinosis

GI EARLY elevated liver enzymes with hepatomegaly LATER cirrhosis and increased risk of
hepatocellular carcinoma

Cardiac Restrictive or dilated cardiomyopathy and conduction abnormalties

Endocrine Diabetes Mellitus, 2 hypogonadism (decreased libido, erectile dysfunction) and

hypothyroidism
Infections- increased risk of Listeria, Vibrio vulnificus, and Yersinia enterocolitica

Dx. Look at iron studies.

Tx. Serial phlebotomy to deplete iron stores.

Legionnaires Disease (Legionella)

Path: Traveling patient comes into contact with contaminated water on a Cruise or Hotel or Hospital.

Px: Fever, GI symptoms: n/v,diarrhea, hyponatremia, headache/confusion, pulmonary symptoms with

interstitial infiltrates, bradycardia

Dx. 1st line Urine Legionella antigen test.

Recall you need charcoal yeast extract, with iron and cysteine to culture and SILVER stain to stain. So a
gram stain that shows PMN but no organisms is suggestive.

Tx. Fluoroquinolones eg Levofloxacin or Macrolides

Amoxicillin/clauvante is used to treat sinusitis, otitis media, and CAP.

Ceftriaxone is good against pneumococcus, haemophilus, and Moraxella.

ARDS

Risk factors: Infection, trauma, massive transfusion, and acute pancreatitis (pancreatic enzymes enter
blood and damage pulmonary capillaries)

Path: Lung injury causes fluid/cytokine leakage into alveoli. This fluid impairs gas exchanged and
decrease lung compliance and can cause pulmonary HTN.

Px: dyspnea, tachypnea, and hypoxemia with bilateral alveolar infiltrates on CXR

Dx: Clinical: worsening respiratory distress within 1 week of insult - Acute Respiratory Distress

Bilateral lung opacities on CXR; not due to CHF Diffusion barrier/diffuse infiltrates
 Hypoxemia with a PaO2/FiO2 < 300 Respiratory Distress

Tx Mechanical ventilation with low TV but HIGH PEEP (Positive End Expiratory Pressure) to keep alveoli
stented open and permissive hypercapnia

- Low TV decreases risk of overdistening alveoli and improve mortality (MOST IMPORANT)
- Give enough O2 to reach 88-95% O2 sat. Do not go less than 88 and dont go higher than 92.
o 88-95% = 55-80 mmHg of O2
- PEEP at 15-20 cm H20 to maintain oxygenation. Hypercapnia is OK.

Lactose Intolerance

Path: as people age, concentration of lactase decreases and pt unable to absorb lactose, which allows
bacteria to metabolize causing diarrhea, cramps, bloating, and flatulence

RF: Asian American, African, Latin, Native American (IE NOT white)

Px: diarrhea, cramps, bloating, and flatulence after consuming dairy products

Dx: hydrogen breath test where pt given lactose and if metabolized by bacteria results in INCREASED
hydrogen levels.

Tx. Avoid dairy products or supplement with lactase.

Urine test for reducing substances is used in patients with glucosuria, galactosuria etc

All forms of OSMOTIC diarrhea (as in lactose intolerance) have a high osmotic gap.

Acid steatocrit is a test for fat malabsorption.

Dermatitis Herpetiformis

Path: associated with vacci disease

Px intensely pruritic, erythematous papules, bullae that are symmetrically grouped and cluster on
elbows, knees, back, and buttocks.

Dx skin biopsy show subepidermal microabscesses at tips of dermal papillae. Immunofluorescence show
deposits of anti transglutaminase igA in dermis
Tx. Initial tx Dapsone. Long-term tx is gluten free diet

25 pt with weight loss and diarrhea, px with intensely itching and burning rash on buttocks.

Herpes Zoster occurs in dermatomal distribution AND is NOT bilateral

Pemphigus vulgaris and Bullous pemiphigoid are autoimmune diseases that usually affected older
individuals.

Cervical Spondylosis

Path

Px. neck pain, limited neck rotation and lateral bending, sensory deficits 2/2 osteophytes radiculopathy.

Dx. Bony spurs (osteophytes) and sclerotic facet joints, narrowing of disk spaces, hypertrophic vertebral
bodies

Liver Cirrhosis

Px

1) Portal HTN symptoms

a. Esophageal varices, Caput medusa, Anorectal varices,
b. Ascites
c. Splenomegaly
2) Hyperestrinism/hypogonadism
a. Spider angiomata, Palmar erythema
b. Gynecomastia (bilat or unilat), Loss of sexual hair, Testicular atrophy
3) Hepatic Synthetic Dysfunction
a. Echhymosis 2/2 to loss of clotting factors
b. Edema

Labs

Euthyroid Status- Because the amount of thyroxine globulin binding hormone is reduced with liver
failure, TOTAL T3/T4 will be reduced but free T3/T4 will be normal. Recall that thyroid releasing system
recalibrates to have exactly the right amount of T3/T4 regardless of the situation

Hashimoto Thyroiditis

Path: autoimmune disease where ab are made against thyroid peroxidase and thyroglobulin preventing
T3/T4 synthesis and HYPOthyroidism

Px: hypothyroidism with enlarged non-tender thyroid gland

Labs: TSH elevated, decreased T4. Ab against thyroid peroxidase

Tx: Synthroid

Peritonsillar Abscess

Path: infection (tonsillitis) that becomes an abscess.

Px: muffled or hot-potato voice, deviation of the uvula, unilateral lymphadenopathy

can be fatal if it obstructs airway or spreads into parapharyngeal space and involve carotid sheath

Tx. Aspiration of the peritonsilar abscess and IV abx

You treat tonsiopharyngitis with a throat swab and oral abx. But when it becomes an abscess you treat
more aggressively.

Epiglottitis can also present with difficulty swallowing and muffled voice but you would NOT see
deviation of the uvula or unilateral lymphadenopathy.

Pulmonary Function Testing

FEV1 = Forced Expiratory Volume in 1 second

FVC = Forced Vital Capacity

1. Look at the FEV1/FVC ratio

a. A low FEV1/FVC ratio points to OBSTRUCTIVE Lung disease
i. A normal/increased DLCO indicates Asthma
ii. A decreased DLCO indicates Emphysema or Chronic bronchitis (COPD)
b. A normal/high FEV1/FVC ratio points to RESTRICTIVE lung disease
i. A normal DLCO indicates Chest wall weakness 2/2 to obesity hypoventilation
syndrome, myasthenia gravis, ALS
ii. A decreased DLCO indicates ILD(interstitial lung disease 2/2 fibrosis)

Emphysema = smoking induced alveolar destruction and hyperinflation

Chronic bronchitis = smoking induced hypertrophy of mucous glands and development of excess
mucous and mucous plugs

ILD includes Pneumoconioses

Hypercalcemia
Path: Causes: Undiagnosed malignancy,

Px: Stones (kidney stones), Bones (bone pain), Groans (abd pain), Thrones (increased urination), and
Psychic overtones (confusion, stupor, coma). Pt are usually dehydrated due to polyuria and decreased
oral intake.

Dx. Ca 2+ level > 11

Tx

1) Severe Hypercalcemia is defined as > 14 mg/dl or a patient with hypercalcemia who is symptomatic.

Short term tx: Normal saline and Calcitonin; avoid loop diuretics unless pt also has HF

Long term tx: Bisphosphonate (zoledronic acid)

2) Moderate Hypercalecmia defined as 12-14 mg/dl

Usually no short-term treatment needed unless symptomatic which is NS + calcitonin

3) Asymtomatic or mild hypercalcemia defined as < 12 mg/ld

No short term treatment, avoid Thiazide diuretics, Lithium, volume depletion, and prolonged
bed rest.

Multiple Myeloma (MM) presents with severe hypercalcemia and pancytopenia.

Routine use of loop diuretics Furosemide is not recommend in hyperglycemia as it can actually worsen
volume depletion.

Hemodialysis is used to treat hypercalcemia in patients with CKD or heart failure who cant receive
aggressive IV NS.

Evaluation of suspected Ventilator Associated Pneumonia

Pt on a ventilator develops pulmonary symptoms and has an abnormal CXR

1) First step is Culture lower respiratory tract tube sample

2) 2nd step is to Start Empiric Abx: You want gram + and gram - coverage, Anti-pseudomonas, and
consider MRSA
a. If cultures come back Positive and patient clinically improves Narrow abx according to
culture results
b. If cultures come back Positive and patient DOES not clinically improve Change antibiotics
and assess for VAP complications such as abscess/ evaluate other causes
c. If cultures come back negative stop Broad spec Abx and look for other causes

VAP (Ventilator Associated Pneumonia)

Path: #1 Pseudomonas, and other gram (e. coli, klebsiella) and gram + S aureus)
Px. Nosocomial PNA that develops 2 days or more after intubation. Fever, purulent secretions,
leukocytosis and issues with ventilation (increased RR, decreased TV)

Dx 1st line CXR, 2nd Culture secretion.

Tx 3rd Start broad spec abx

CT scan can be used to look for complications if the patient does not improve after starting abx.

Takayasu Arteritis

Path: large artery vasculitis that involves branch points of the Aortic arch

RF: Female, Asian, under age 50 (10-40s)

Px: Arterio-occlusive disease in UE: claudication( eg exertional arm pain), ulcers, arthralgia,
myalgias,

Visual and neurologic symptoms,

Initial symptoms: Constitutional symptoms: fever, weight loss

Physical Exam: unequal BP, pulse deficit, arterial bruits

Dx. Elevated inflammatory markers ESR, CRP

CXR shows Aortic dilatation or widened mediastinum

CT/MRI: wall thickening and narrowing of lumen

Tx: Systemic glucocorticoids

Aortic coarctation would cause pulse and blood pressure deficits in the LE, not the UE. More common in
babies and kids and does not cause INFLAMMATORY symptoms.

Giant cell arteritis affects women > 50. Presents with temporal or scalp tenderness and chronic pain and
stiffness of shoulders: polymyalgia Rheumatica.

Buerger disease or Thromoangitis Obliterans is a vasculitis that occurs in MEN SMOKERS and presents
with superficial thrombophlebitis (blockage of superficial veins) and ischemia/gangrene of digits.

Ascites

Tx

Loop diuretics eg Furosemide and can include spironolactone

Loop diuretics can cause contraction-alkalosis with Hypokalemia. Increased Na+ delivery to distal tubule
increased secretion of H+ and K+, low blood volume triggers Aldo which stimulates even more H+ and K+
loss.

Acute kidney injury causes anion gap metabolic acidosis and Hyperkalemia.

Metabolic Alkalosis

Path/Causes: excess production of bicarb (generation phase) and inability to excrete bicarb
(maintenance phase)

Saline Responsive: Vomiting, GI suctioning, Diuretics, laxative use, Volume depletion

Saline Unresponsive is 2/2 to mineralocorticoid driving H+ and K+ secretion and Na+ reabsorption which
leads to increased extracellular volume. Kidneys ultimately respond by excreting Na+ and chloride,
generating Urine chloride > 20 mEq/L.

Saline Unresponsive: Primary Hyperaldosteronism, Cushing syndrome, severe hypokalemia

Px volume depletion, hypokalemia with muscle weakness, arrhythmias, muscle cramps

Dx Urine chloride to determine if saline responsive or resistant

Tx treat underling cause to reverse generation phase. Saline responsive give Normal saline.

Chronic vomiting can cause Metabolic Alkalosis, Hypokalemia, and Hypochloremia

Acute Liver Failure

Path: Causes: Viral, drug toxicity eg acetaminophen, ischemia (shock liver or budd-chiari syndrome),
autoimmune hepatitis, wilson disease, malignancy

Px: RUQ pain, generalized symptoms: fatigue lethargy etc, Jaundice and pruritus, Thrombocytopenia,
Hypoglycemia, Renal insufficiency , hepatic encephalopathy (confusion, asterixis)

Dx Severe acute liver injury is when AST/ALT are > 1000 U/L, signs of hepatic encephalopathy: confusion
and Asterixis, INR > 1.5

Alcohol and Acetaminophen are a bad combo.

Acute alcoholic hepatitis presents with AST/ALT < 500. And the AST/ALT ratio should be > 2. at least 2
glasses of Scotch

Budd-chiari presents with signs of Acute Liver failure + SEVERE RUQ pain.

Hemophilia
Path: X-linked so affects MEN, not women. As opposed to vWF which affects Men and Women and
causes mucosal bleeding so: menorrhagia.

Px: delayed/prolonged bleeding after mild trauma or a procedure

1. Hemathrosis
2. Intramuscular hematomas
3. GI or GU tract bleeding

Lab findings; Prolonged PTT, but normal PT, nomrmal platelet count, bleeding time etc

Decreased factor 8 or 9

Tx: Give recombination factor 8 or 9. For Hemophilia A give Desmopressin

Hereditary Telangiectasis autosomal dominant disorder with recurrent epistaxis and telangeictasis.

JC Virus

Path: affects immunocompromised patients (reactivation attacks oligodendrocytes white matter

demyelination ) HIV patients with CD4 < 200.

Px: slowly progressive, neurologic symptoms: confusion, paresis, ataxia, diplopia seizure

Dx: MRI brain showing white matter lesions that are NON-enhancing with no surrounding edema, LP
with CSF PCR for JV virus, Brain bx (rarely done)

Tx: Restart HAART therapy; usually fatal

Cerebral Toxo would px with multiple-ring ENHANCING lesions with EDEMA

Primary CNS lymphoma presents with a SINGLE, well defined, enhacing lesion.

HIV associated dementia affects deep gray matter structures, causing subacute cognitive, behavioral,
and motor deficits. Imaging would show cerebral atrophy with ventricular enlargement

SSPE would show brain scarring and atrophy

Ethical Questions

1. A patient dx with meningococcal meningitis who is highly contagious should be encouraged to be

hospitalized and if he refuses should be hospitalized and treated against his will.
The key point here is that the patient poses a harm to himself and others and so he should be
involuntarily admitted if needed. In general, an adult with decision making capacity has the
right to refuse life-saving treatment as long as the patient DOES not put others at risk eg the
patient has a highly communicable disease as in this case.
 2. Communication failures during sign out and handoff have been linked to adverse clinical events.
Best way to address this is a sign-out checklist. Sign-out should be done verbally with a written
component, face-to-face with minimal interruption.
3. A narcissistic patient with cough (non-urgent concern) comes to your clinic after hour and
demands that he be seen (inappropriate demand). How should you respond? Tell the patient to
come back tomorrow during office hours as his condition is not an emergency. DO NOT send
him to the ED as this would be a waste of resources. Key points are 1) set limits 2) be
professional: its not ok to see a patient after office hours unless it is an emergency but do not
forget to address their concern: I know you have a cough but it can wait till tomorrow.
4. A patient dies and the attending asks if you want to practice procedures on the dead patient.
What should you do? Once you obtain permission from the patients family, you can practice
the procedures under close supervision. It is ethical for students to practice on deceased
patients as long as they have permission from the patient before dying or family. However, if
patients consent wasnt document or there are no family members around ie (no permission)
you cannot.
5.

Biostats Questions

The ways to reduce Confounding are Crossover Multiple studies, Matching, Randomization, Restriction.
At the analysis stage you can reduce confounding with Stratified analysis and Statistical modeling.

Restriction is when you restrict study participants to the confounder. Ie being a male is a confounder in
a study so all the patients selected are male.

Post-hoc analysis is when unplanned statistical tests are performed on data from a completed study and
can lead to incorrect conclusions.

Selective survival bias occurs in case-control studies where cases are selected from the entire disease
population instead of patients who are newly diagnosed. Eg. Looking at cancer survival in all patients vs
newly diagnosed patients. The cancer patients who are not newly diagnosed and are alive at the study
probably a more benign cancer and are more likely to live.

Proper phrasing for a null hypothesis is There is no association between the exposure and outcome.
Buzz words are no association. To get it completely right also take into account the study design. A
cross-sectional study can measure prevalence, a cohort measures incidence/relative risk etc.
The best study to determine incidence is Cohort

Incidence (the # of individuals who develop a disease in a population) /(risk) = Cohort

Prevalence (the total # of cases in a population) = Cross-sectional studies

Odds-ratio = Case-Control Studies look at associations b/w risk factors and disease occurrence.

A case series is a study involving ONLY patients who already have the disease of interest. It is used to
determine the natural history of uncommon conditions.

A clinical trial compares the therapeutic benefit of different interventions in patients already diagnosed
with a particular disease.

Susceptibility bias is a selection bias whereby patients are selected for a certain intervention based on
the severity of their condition. Address by using an Intention to Treat study where regardless of what
the final groups are: ie no intervention switches to intervention at end of study, data is analyzed with
the original treatment group configuration.