Académique Documents
Professionnel Documents
Culture Documents
SEC TION II
BEHAVIORAL SCIENCE
``
BEHAVIORAL SCIENCEPUBLIC HEALTH
MEASURE
EXAMPLE
Outcome
Impact on patients
Process
Balancing
New
Figure
Preconditions
Unsafe acts
Types of medical
New errors
Fact
Harm
Active error
Immediate impact.
Latent error
Revised
Figure
66
SEC TION II
Flow cytometry
BIOCHEMISTRY
``
BIOCHEMISTRYLABORATORY TECHNIQUES
New
Fact
Cell
Anti-CD3 Ab
Anti-CD8 Ab
Laser
Fluorescence
is detected;
labeled cells
are counted
Microarrays
Laser makes
label fluoresce
tor
tec
De
104
103
CD3
Revised
Figure
4th
draft
Antibody
102
101
100
100
101
102
103
104
CD8
Thousands of nucleic acid sequences are arranged in grids on glass or silicon. DNA or RNA probes
are hybridized to the chip, and a scanner detects the relative amounts of complementary binding.
Used to profile gene expression levels of thousands of genes simultaneously to study certain diseases
and treatments. Able to detect single nucleotide polymorphisms (SNPs) and copy number
variations (CNVs) for a variety of applications including genotyping, clinical genetic testing,
forensic analysis, cancer mutations, and genetic linkage analysis.
New
Figure
BIOCHEMISTRY
SEC TION II
``
BIOCHEMISTRYMETABOLISM
Summary of pathways
Galactose metabolism
Galactokinase (mild galactosemia)
New
Figure
Galactose-1-phosphate
uridyltransferase
(severe galactosemia)
Galactose
Glycogen
Glucose
Galactose-1-phosphate
Glycolysis
Hexokinase/glucokinase
Glucose-6-phosphatase
(von Gierke disease)
Glucose-6-phosphate
dehydrogenase
HMP shunt
UDP-glucose
Glucose-1-phosphate
Glucose-6-phosphate
6-phosphogluconolactone
Glycogenesis / glycogenolysis
Ribulose-5-phosphate
Fructose-6-phosphate
Gluconeogenesis
Transketolase
Fructose metabolism
Fructose-1,6-bisphosphate
Phosphofructokinase-1
Fructose-1,6-bisphosphatase
Fructokinase (essential fructosuria)
Fructose-1-phosphate
DHAP
Glyceraldehyde-3-P
Fructose
1,3-bisphosphoglycerate
Glycerol
2-phosphoglycerate
Triglycerides
Phosphoenolpyruvate (PEP)
Fatty acids
Citrate synthase
Isocitrate dehydrogenase
Pyruvate
-ketoglutarate dehydrogenase
Lactate
Cholesterol
Malonyl-CoA
Ornithine transcarbamylase
Lipid metabolism
3-phosphoglycerate
Acetyl-CoA
Mevalonate
Propionyl-CoA carboxylase
Acetoacetyl-CoA
HMG-CoA
Acetoacetate
Citrate
Aspartate
NH3 + CO2
Oxaloacetate
Citrulline
Argininosuccinate
Carbamoyl phosphate
Ornithine
Urea cycle
Arginine
Urea
H2O
-hydroxybutyrate
Isocitrate
Ketogenesis
Malate
TCA cycle
-ketoglutarate
Fumarate
Succinate
Succinyl-CoA
B12
Methylmalonyl-CoA
Propionyl-CoA
Protein metabolism
85
118
SEC TION II
MICROBIOLOGY
``
MICROBIOLOGYCLINICAL BACTERIOLOGY
``
MICROBIOLOGYCLINICAL BACTERIOLOGY
Gram-positive lab algorithm
Gram
(purple/blue)
Shape
Bacilli
Swapped
Figure
Branching
filaments
Cocci
Aerobic
Anaerobic
Listeria
Bacillus
Corynebacterium
Clostridium
Aerobic
Aerobic
Anaerobic
Nocardia
(acid fast)
Actinomyces
(not acid fast)
Catalase
Revised
Figure
Streptococcus
Staphylococcus
Hemolysis
Coagulase
(Partial
hemolysis,
green)
Optochin sensitive
and bile soluble
Bacitracin sensitivity
Group B
S agalactiae
Viridans streptococci
(no capsule)
S mutans
S mitis
(Complete
hemolysis,
clear)
(No hemolysis,
grows in bile)
Group A
S pyogenes
S pneumoniae
(encapsulated)
Novobiocin
sensitivity
Nonenterococcus
S bovis
S saprophyticus
S aureus
S epidermidis
Group D
(enterococcus)
E faecium
E faecalis
NOvobiocinSaprophyticus is Resistant;
Epidermidis is Sensitive.
Streptococci
OVRPS (overpass).
B-BRAS.
MICROBIOLOGY
Corynebacterium
diphtheriae
A
Listeria
monocytogenes
A
Gram , facultative intracellular rod; acquired by ingestion of unpasteurized dairy products and
cold deli meats, via transplacental transmission, or by vaginal transmission during birth.
Forms rocket tails (red in A ) via actin polymerization that allow intracellular movement and cellto-cell spread across cell membranes, thereby avoiding antibody. Characteristic tumbling motility
in broth; is only gram organism to produce endotoxin.
Can cause amnionitis, septicemia, and spontaneous abortion in pregnant women; granulomatosis
infantiseptica; neonatal meningitis; meningitis in immunocompromised patients; mild, selflimited gastroenteritis in healthy individuals.
Treatment: ampicillin in infants, immunocompromised, and the elderly as empirical treatment of
meningitis.
Nocardia
Actinomyces
Aerobe
Anaerobe
Found in soil
image
image
123
Both are gram and form long, branching filaments resembling fungi.
Color
Color
SEC TION II
Nocardia vs
Actinomyces
adjusted
adjusted
``
MICROBIOLOGYCLINICAL BACTERIOLOGY
216
SEC TION II
PATHOLOGY
``
PATHOLOGYINFLAMMATION
``
PATHOLOGYINFLAMMATION
Apoptosis
ATP-dependent programmed cell death. Intrinsic or extrinsic pathway; both pathways activation
of cytosolic proteases called caspases that mediate cellular breakdown cell shrinkage,
chromatin condensation, membrane blebbing, and formation of apoptotic bodies, which are then
phagocytosed.
Characterized by deeply eosinophilic cytoplasm and basophilic nucleus, pyknosis (nuclear
shrinkage), and karyorrhexis (fragmentation caused by endonucleases cleaving at
internucleosomal regions). DNA laddering (fragments in multiples of 180 bp) is a sensitive
indicator of apoptosis.
Cell membrane typically remains intact without significant inflammation (unlike necrosis).
Intrinsic
(mitochondrial)
pathway
Extrinsic (death
receptor) pathway
2 pathways:
Ligand receptor interactions (FasL binding to Fas [CD95] or TNF- binding to TNF)
Immune cell (cytotoxic T-cell release of perforin and granzyme B)
Fas-FasL interaction is necessary in thymic medullary negative selection. Mutations in Fas
numbers of circulating self-reacting lymphocytes due to failure of clonal deletion.
Defective Fas-FasL interactions cause autoimmune lymphoproliferative syndrome.
Intrinsic
(mitochondrial) pathway
Extrinsic
(death receptor) pathway
FasL
Fas
DNA damage
Radiation, ROS, toxins
Misfolded proteins
Hypoxia
Initiator
caspases
p53 activation
New
Figure
Cytochrome C
BAX/BAK
Bcl-2
Executioner
caspases
Granzyme
Perforin
Nuclear
fragmentation
APAF-1
Macrophage
Initiator
caspases
Cytoskelet
al dispersion
Revised
Figure
Cytotoxic T cell
Cytoplasmic
bleb
Ligands for
macrophage cell
receptors
Apoptotic
body
300
CARDIOVASCULAR
``
CARDIOVASCULARPHARMACOLOGY
Lipid-lowering agents
DRUG
LDL
HDL
TRIGLYCERIDES
MECHANISMS OF ACTION
ADVERSE EFFECTS/PROBLEMS
Hepatotoxicity ( LFTs),
myopathy (esp. when used
with fibrates or niacin)
HMG-CoA reductase
inhibitors
(eg,lovastatin,
pravastatin)
Slightly
Slightly
GI upset, absorption of
other drugs and fat-soluble
vitamins
Ezetimibe
Fibrates
(gemfibrozil,
bezafibrate,
fenofibrate)
Upregulate LPL TG
clearance
Activates PPAR- to induce
HDL synthesis
Revised
Figure
Liver
Blood
Enterocyte
Intestinal lumen
Acetyl CoA
Apo E
receptor
HMG-CoA
New
Figure
HMG-CoA
reductase
Triacylglyceride
Mevalonate
MEVALONATE
SYNTHESIS
CHY
rem
VLDL
FFA
Cholesterol
FFA
Bile acids
VLDL
LPL
HDL
receptor
HDL
FFA
HDL
FFA
LDL
LDL
receptor
LDL
CHOLESTEROL
ABSORPTION
Ezetimibe
Niacin
Statins
Lovastatin
Pravastatin
Simvastatin
Atorvastatin
Rosuvastatin
CHY
LPL
HDL
pool
Cholesterol
Lymphatics
CHY
Lipolysis
Adipose tissue
LPLUPREGULATION
Fibrates
gemfibrozil
bezafibrate
fenofibrate
ADIPOSE LIPOLYSIS
Niacin
Cholesterol
FFA
Bile acids
BILE ACID
REABSORPTION
Bile acid resins
cholestyramine
colestipol
colesevelam
ENDOCRINE
``
ENDOCRINEPHARMACOLOGY
335
ACTION
CLINICAL USE
RISKS/CONCERNS
Used as monotherapy in
type2 DM or combined
with metformin.
GLP-1 analogs
glucose-dependent insulin release, Type 2 DM.
Exenatide,
glucagon release, gastric
liraglutide (sc injection)
emptying, satiety.
Nausea, vomiting,
pancreatitis; modest
weight loss.
DPP-4 inhibitors
Linagliptin,
saxagliptin,
sitagliptin
Type 2 DM.
Amylin analogs
Pramlintide
(scinjection)
Sodium-glucose
co-transporter 2
(SGLT-2) inhibitors
Canagliflozin,
dapagliflozin,
empagliflozin
Type 2 DM.
Glucosuria, UTIs,
vaginal yeast infections,
hyperkalemia, dehydration
(orthostatic hypotension).
-glucosidase
inhibitors
Acarbose,
miglitol
Type 2 DM.
GI disturbances.
aGenes
activated by PPAR- regulate fatty acid storage and glucose metabolism. Activation of PPAR- insulin sensitivity and
levels of adiponectin.
Thionamides
MECHANISM
Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of
iodine inhibition of thyroid hormone synthesis. Propylthiouracil also blocks 5-deiodinase
peripheral conversion of T4 to T3.
CLINICAL USE
ADVERSE EFFECTS
CLINICAL USE
ADVERSE EFFECTS
342
GASTROINTESTINAL
``
GASTROINTESTINALANATOMY
Left
T12
IVC
Middle suprarenal
Celiac
trunk
First lumbar
L1
Superior
mesenteric
Renal
Gonadal (testicular/ovarian)
L2
Second lumbar
L3
Third lumbar
New
Figure
Revised
Figure
Inferior
mesenteric
L4
Fourth lumbar
Bifourcation at L4
ac
i
on
mm
co
c
lia
Rig
ht
co
mm
on
ili
ft
Le
L5
Median sacral
artery
Right internal
iliac
Left internal
iliac
ARTERY
PARASYMPATHETIC
INNERVATION
VERTEBRAL
LEVEL
Foregut
Celiac
Vagus
T12/L1
Midgut
SMA
Vagus
L1
Hindgut
IMA
Pelvic
L3
STRUCTURES SUPPLIED
GASTROINTESTINAL
Wilson disease
(hepatolenticular
degeneration)
A
Color
adjusted
image
Hemochromatosis
A
Revised
Fact
Color
adjusted
image
``
GASTROINTESTINALPATHOLOGY
371
Recessive mutations in HFE gene (C282Y > H63D, chromosome 6) abnormal iron sensing and
intestinal absorption (ferritin, iron, TIBC transferrin saturation). Iron overload can
also be 2 to chronic transfusion therapy (eg, -thalassemia major). Iron accumulates, especially in
liver, pancreas, skin, heart, pituitary, joints. Hemosiderin (iron) can be identified on liver MRI or
biopsy with Prussian blue stain A .
Presents after age 40 when total body iron > 20 g; iron loss through menstruation slows progression
in women. Classic triad of cirrhosis, diabetes mellitus, skin pigmentation (bronze diabetes). Also
causes dilated cardiomyopathy (reversible), hypogonadism, arthropathy (calcium pyrophosphate
deposition; especially metacarpophalangeal joints). HCC is common cause of death.
Treatment: repeated phlebotomy, chelation with deferasirox, deferoxamine, oral deferiprone.
May present with pruritus, jaundice, dark urine, light-colored stool, hepatosplenomegaly. Typically
with cholestatic pattern of LFTs (conjugated bilirubin, cholesterol, ALP).
PATHOLOGY
EPIDEMIOLOGY
ADDITIONAL FEATURES
Primary sclerosing
cholangitis
Primary biliary
cirrhosis
Autoimmune reaction
lymphocytic infiltrate
+granulomas destruction
of intralobular bile ducts.
Classically in middle-aged
women.
Secondary biliary
cirrhosis
Anti-mitochondrial antibody,
IgM. Associated with other
autoimmune conditions
(eg, Sjgren syndrome,
Hashimoto thyroiditis,
CREST, rheumatoid arthritis,
celiac disease).
``
HEMATOLOGY AND ONCOLOGYPHYSIOLOGY
383
Hemoglobin electrophoresis
On a gel, hemoglobin migrates from the
negatively charged cathode to the positively
charged anode. HbA migrates the farthest,
followed by HbS, followed by HbC. This is
because the missense mutations in HbS and
HbC replace glutamic acid with valine
(neutral) and lysine , respectively, impacting
the net protein charge.
Origin
Hb C trait
AC
SS
AS
Normal newborn
AF
New
Fact
Normal adult
AA
Hb C disease
SC
Hb SC disease
CC
C
Cathode
A
Anode
Revised
Figure
VII
Tissue factor
XII
XIIa
XI
Pain
XIa
ANTICOAGULANTS: factor Xa
- LMWH (greatest efficacy)
- heparin
- direct Xa inhibitors (apixaban, rivaroxaban)
- fondaparinux
IXa
VIII
with vWF)
VIIIa
Xa
Va
II
IIa
Prothrombin Thrombin
Plasminogen
Ia
I
Fibrinogen Fibrin monomers
tPA
Aggregation
Permeability
Kinin cascade
*
VIIa
Vasodilation
Bradykinin
IX
Tissue factor
(extrinsic)
pathway
HMWK
Kallikrein
Plasmin
Combined
pathway
Ca2+
XIIIa
THROMBOLYTICS:
alteplase, reteplase,
streptokinase, tenecteplase
Aminocaproic acid
Fibrinolytic system
XIII
Fibrin degradation
products
402
Leukemias
``
HEMATOLOGY AND ONCOLOGYPATHOLOGY
Unregulated growth and differentiation of WBCs in bone marrow marrow failure anemia
(RBCs), infections ( mature WBCs), and hemorrhage ( platelets). Usually presents with
circulating WBCs (malignant leukocytes in blood); rare cases present with normal/WBCs.
Leukemic cell infiltration of liver, spleen, lymph nodes, and skin (leukemia cutis) possible.
TYPE
NOTES
Lymphoid neoplasms
Acute lymphoblastic
leukemia/lymphoma
Most frequently occurs in children; less common in adults (worse prognosis). T-cell ALL can
present as mediastinal mass (presenting as SVC-like syndrome). Associated with Down syndrome.
Peripheral blood and bone marrow have lymphoblasts A .
TdT+ (marker of pre-T and pre-B cells), CD10+ (marker of pre-B cells).
Most responsive to therapy.
May spread to CNS and testes.
t(12;21) better prognosis.
Chronic lymphocytic
leukemia/small
lymphocytic
lymphoma
Age: > 60 years. Most common adult leukemia. CD20+, CD5+ B-cell neoplasm. Often
asymptomatic, progresses slowly; smudge cells B in peripheral blood smear; autoimmune
hemolytic anemia. CLL = Crushed Little Lymphocytes (smudge cells).
Richter transformationSLL/CLL transformation into an aggressive lymphoma, most commonly
diffuse large B-cell lymphoma (DLBCL).
Age: Adult males. Mature B-cell tumor. Cells have filamentous, hair-like projections
(fuzzy appearing on LM C ).
Causes marrow fibrosis drytap on aspiration. Patients usually present with massive
splenomegaly.
Stains TRAP (tartrate-resistant acid phosphatase). TRAP stain largely replaced with flow
cytometry.
Treatment: cladribine, pentostatin.
Myeloid neoplasms
Acute myelogenous
leukemiaa
Median onset 65 years. Auer rods D ; myeloperoxidase cytoplasmic inclusions seen mostly in
APL (formerly M3 AML); circulating myeloblasts on peripheral smear; adults.
Risk factors: prior exposure to alkylating chemotherapy, radiation, myeloproliferative disorders,
Down syndrome. t(15;17) APL subtype responds to all-trans retinoic acid (vitamin A), inducing
differentiation of promyelocytes; DIC is a common presentation.
Chronic myelogenous
leukemia
Occurs across the age spectrum with peak incidence 4585 years, median age at diagnosis 64 years.
Defined by the Philadelphia chromosome (t[9;22], BCR-ABL) and myeloid stem cell proliferation.
Presents with neutrophils, metamyelocytes, basophils E , and splenomegaly. May accelerate and
transform to AML or ALL (blast crisis).
Very low LAP as a result of low activity in malignant neutrophils (vs benign neutrophilia
[leukemoid reaction], in which LAP is ).
Responds to bcr-abl tyrosine kinase inhibitors (eg, imatinib).
A,B,C
= Color
adjusted
image
C&E=
Swapped
Images
NEUROLOGY
``
NEUROLOGYANATOMY AND PHYSIOLOGY
469
Intracranial hemorrhage
Epidural hematoma
Rupture of middle meningeal artery (branch of maxillary artery), often 2 to skull fracture A .
Lucid interval. Rapid expansion under systemic arterial pressure transtentorial herniation, CN
III palsy.
CT shows biconvex (lentiform), hyperdense blood collection B not crossing suture lines.
Subdural hematoma
Rupture of bridging veins. Can be acute (traumatic, high-energy impact hyperdense on CT) or
chronic (associated with mild trauma, cerebral atrophy, elderly, alcoholism hypodense on CT).
Seen in shaken babies. Predisposing factors: brain atrophy, trauma.
Crescent-shaped hemorrhage that crosses suture lines (red arrows in C and D ). Can cause midline
shift (blue arrow in C ), findings of acute on chronic hemorrhage (blue arrow in D ).
Subarachnoid
hemorrhage
Intraparenchymal
hemorrhage
Most commonly caused by systemic hypertension. Also seen with amyloid angiopathy (recurrent
lobar hemorrhagic stroke in elderly), vasculitis, neoplasm. May be 2 to reperfusion injury in
ischemic stroke. Typically occurs in basal ganglia G and internal capsule (Charcot-Bouchard
aneurysm of lenticulostriate vessels), but can be lobar H .
A
A,B,C,D,
E,F,G =
Color
E=
adjusted
Swapped
image
Image
E
DE=
E=
revised
Swapped
images
Figure
NEUROLOGY
``
NEUROLOGYPATHOLOGY
491
``
NEUROLOGYPATHOLOGY
Dementia
DISEASE
DESCRIPTION
HISTOLOGIC/GROSS FINDINGS
Alzheimer disease
Frontotemporal
dementia
Vascular dementia
Creutzfeldt-Jakob
disease
Spongiform cortex.
Prions (PrPc PrPsc sheet [-pleated sheet
resistant to proteases]).
Other causes
B=
New
Image
A,C =
Color
adjusted
image
PSYCHIATRY
``
PSYCHIATRYPATHOLOGY
Panic disorder
Specific phobia
Severe, persistent fear or anxiety due to presence or anticipation of a specific object or situation.
Person recognizes fear is excessive. Can be treated with systematic desensitization.
517
PANICS.
Diagnosis requires attack followed by 1 month
(or more) of 1 (or more) of the following:
Persistent concern of additional attacks
Worrying about consequences of attack
Behavioral change related to attacks
Symptoms are the systemic manifestations of
fear.
Generalized anxiety
disorder
Anxiety lasting > 6 months unrelated to a specific person, situation, or event. Associated with
restlessness, irritability, sleep disturbance, fatigue, muscle tension, difficulty concentrating.
Treatment: CBT, SSRIs, SNRIs are first line. Buspirone, TCAs, benzodiazepines are second line.
Adjustment disorderemotional symptoms (anxiety, depression) causing impairment following
an identifiable psychosocial stressor (eg, divorce, illness) and lasting < 6 months (> 6 months in
presence of chronic stressor). Treatment: CBT, SSRIs.
Obsessive-compulsive
disorder
Recurring intrusive thoughts, feelings, or sensations (obsessions) that cause severe distress;
relieved in part by the performance of repetitive actions (compulsions). Ego-dystonic: behavior
inconsistent with ones own beliefs and attitudes (vs obsessive-compulsive personality disorder).
Associated with Tourette syndrome. Treatment: CBT, SSRIs, and clomipramine are first line.
Body dysmorphic disorderpreoccupation with minor or imagined defect in appearance
significant emotional distress or impaired functioning; patients often repeatedly seek cosmetic
treatment. Treatment: CBT.
Post-traumatic stress
disorder
Exposure to prior trauma (eg, death, serious injury, rape) intrusive reexperiencing of the event
(nightmares, flashbacks), avoidance of associated stimuli, changes in cognition or mood (fear,
horror), and persistently arousal. Disturbance lasts >1month with significant distress or
impaired social-occupational functioning. Treatment: CBT, SSRIs, and venlafaxine are first line.
Acute stress disorderlasts between 3 days and 1 month. Treatment: CBT; pharmacotherapy is
usually not indicated.
RENAL
``
RENALPHYSIOLOGY
541
1,25-(OH)2 D3
1-hydroxylase
1,25-(OH)2 D3
+
PTH
Prostaglandins
Dopamine
Proximal
convoluted
tubule
Revised
Figure
5th
draft
Distal
convoluted
tubule
Mg2+
Sugars
Amino acids
Na+
Angiotensin II
K+
H+
Synthesized in response to
GFR and FF but with compensatory Na+
constriction
Parathyroid hormone
Cortex
Medulla
Na+
K+
2CI
ADH (vasopressin)
Secreted in response to
plasma osmolarity and
blood volume. Binds to
receptors on principal cells,
causing number of
aquaporins and H2O
reabsorption.
Ascending limb,
loop of Henle
Secreted in response to
plasma [Ca2+], plasma [PO43],
or plasma 1,25-(OH)2 D3.
Causes [Ca2+] reabsorption (DCT),
[PO43] reabsorption (PCT), and
1,25-(OH)2 D3 production
( Ca2+ and PO43 absorption from gut
via vitamin D).
(permeable to salts)
Collecting
duct
Loop of Henle
Aldosterone
Secreted in response to
blood volume (via AT II) and
plasma [K+]; causes Na+
Na+
reabsorption, K+ secretion,
H2O (potentially)
H+ secretion.
Ca2+
Mg2+
Ca2+
RENAL
``
RENALPHYSIOLOGY
Acid-base physiology
pH
PCO2
[HCO3]
COMPENSATORY RESPONSE
Metabolic acidosis
Hyperventilation (immediate)
Metabolic alkalosis
Hypoventilation (immediate)
Respiratory acidosis
Respiratory alkalosis
[HCO3]
0.03 Pco2
Predicted respiratory compensation for a simple metabolic acidosis can be calculated using the
Winters formula. If measured Pco2 > predicted Pco2 concomitant respiratory acidosis; if
measured Pco2 < predicted Pco2 concomitant respiratory alkalosis:
Pco2 = 1.5 [HCO3 ] + 8 2
Acidosis/alkalosis
Check arterial pH
pH < 7.35
Revised
Figure
Acidemia
Pco2 > 44 mm Hg
Respiratory
acidosis
Alkalemia
Pco2 < 36 mm Hg
Respiratory
alkalosis
Metabolic acidosis
Hypoventilation
Airway obstruction
Acute lung disease
Chronic lung disease
Opioids, sedatives
Weakening of respiratory
muscles
> 12 mEq/L
Hysteria
Hypoxemia (eg, high altitude)
Salicylates (early)
Tumor
Pulmonary embolism
812 mEq/L
45
Anion gap
MUDPILES:
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or INH
Lactic acidosis
Ethylene glycol (
oxalic acid)
Salicylates (late)
40
35
Respiratory
acidosis
25
15
10
5
Loop diuretics
Vomiting
Antacid use
Hyperaldosteronism
Metabolic
alkalosis
Pco2 =
40 mm Hg
Mixed
alkalosis
30
20
Metabolic alkalosis
Hyperventilation
New
Figure
pH > 7.45
Mixed
acidosis
Metabolic
acidosis
Buffer line
Respiratory
alkalosis
6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9
pH
543
602
Progestins
REPRODUC TIVE
``
REPRODUCTIVEPHARMACOLOGY
MECHANISM
CLINICAL USE
Contraception (forms include pill, intrauterine device, implant, depot injection), endometrial
cancer, abnormal uterine bleeding. Progestin challenge: presence of withdrawal bleeding
excludes anatomic defects (eg, Asherman syndrome) and chronic anovulation without estrogen.
Antiprogestins
Mifepristone, ulipristal.
MECHANISM
CLINICAL USE
Combined
contraception
Progestins and ethinyl estradiol; forms include pill, patch, vaginal ring.
Estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge. No estrogen surge no
LH surge no ovulation.
Progestins cause thickening of cervical mucus, thereby limiting access of sperm to uterus.
Progestins also inhibit endometrial proliferation endometrium is less suitable to the
implantation of an embryo.
Contraindications: smokers > 35 years old ( risk of cardiovascular events), patients with risk of
cardiovascular disease (including history of venous thromboembolism, coronary artery disease,
stroke), migraine (especially with aura), breast cancer.
MECHANISM
Produces local inflammatory reaction toxic to sperm and ova, preventing fertilization and
implantation; hormone free.
CLINICAL USE
ADVERSE EFFECTS
Heavier or longer menses, dysmenorrhea. Risk of PID with insertion (contraindicated in active
pelvic infection).
Terbutaline, ritodrine
2-agonists that relax the uterus; used to contraction frequency in women during labor.
Danazol
MECHANISM
CLINICAL USE
ADVERSE EFFECTS
608
RESPIRATORY
``
RESPIRATORYANATOMY
``
RESPIRATORYANATOMY
Respiratory tree
Conducting zone
Large airways consist of nose, pharynx, larynx, trachea, and bronchi. Small airways consist of
bronchioles that further divide into terminal bronchioles (large numbers in parallel least airway
resistance).
Warms, humidifies, and filters air but does not participate in gas exchange anatomic dead
space.
Cartilage and goblet cells extend to end of bronchi.
Pseudostratified ciliated columnar cells primarily make up epithelium of bronchus and extend to
beginning of terminal bronchioles, then transition to cuboidal cells. Clear mucus and debris from
lungs (mucociliary escalator).
Airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point).
Respiratory zone
Lung parenchyma; consists of respiratory bronchioles, alveolar ducts, and alveoli. Participates in gas
exchange.
Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli. Cilia
terminate in respiratory bronchioles. Alveolar macrophages clear debris and participate in
immune response.
GROSS
HISTOLOGIC
Conducting zone
Trachea
Basal cell
Goblet cell
Ciliated cell
Pseudostratified
ciliated columnar
epithelium
Smooth muscle
New
Figure
Bronchi
Revised
Figure
Bronchioles
Cartilage
Terminal
bronchioles
Smooth
muscle
Respiratory zone
Respiratory
bronchioles
Cuboidal
ciliated cells
Club cell
Squamous cell
Squamous epithelium
Smooth muscle
Alveolar sacs
Type I pneumocyte
Type II pneumocyte
Alveolar macrophage
Capillary
618
Obstructive lung
diseases
RESPIRATORY
``
RESPIRATORYPATHOLOGY
Obstruction of air flow resulting in air trapping in lungs. Airways close prematurely at high lung
volumes RV and FRC, TLC. PFTs: FEV1, FVC FEV1/FVC ratio (hallmark),
V/Q mismatch. Chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale.
TYPE
PATHOLOGY
OTHER
Chronic bronchitis
(blue bloater)
Emphysema (pink
puffer)
Asthma
hypertrophy is
hyphenated to lose
1 line; to avoid page
being too long
Bronchiectasis
AG =
Color
adjusted
image