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STEP1 > Basics of Pathology > Flashcards

Basics of Pathology Flashcards

1
Q

In what way to permanent tissues respond to stress?

A

hypertrophy only since they are incapable of hyperplasia

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2
Q

Why is pathologic hyperplasia dangerous?

A

it may progress to dysplasia and eventually to cancer

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3
Q

Most pathologic hyperplasias carry a risk of dysplasia and eventually cancer. What is the exception to this?

A

BPH does not carry a risk for prostate cancer

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4
Q

Define atrophy.

A

a response to stress characterized by a decrease in the size and number of cells

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5
Q

What mechanisms underly the decrease in cell number and size that define atrophy?

A
  • decline in cell number is mediated by apoptosis
  • decline in cell size occurs via ubiquitin-proteasome degradation of the cytoskeleton and autophagy of cellular components
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6
Q

What is metaplasia?

A

a change in cell type due to a change in the stress on an organ or tissue

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7
Q

Metaplasia most commonly involves what change?

A

change of one type of surface epithelium to another

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8
Q

What is a classic example of metaplasia?

A

Barrett esophagus

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9
Q

What is Barrett esophagus? What transition occurs? What cancer is it associated with?

A
  • a classic example of metaplasia
  • the esophagus is normally lined by nonkeratinizing squamous epithelium suitable for the friction of a food bolus
  • acid reflux induces a metaplasia to a non-ciliated, mucin-producing columnar epithelium better able to handle the stress of acid
  • poses a risk for adenocarcinoma
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10
Q

Through what mechanism does metaplasia occur?

A

via reprogramming of stem cells

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11
Q

Most metaplasias carry a risk for dysplasia and malignant transformation. What is the exception to this?

A

apocrine metaplasia of the breast carries no increased risk for cancer, rather it is associated with fibrocystic change

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12
Q

Apocrine metaplasia of the breast carries a risk for what?

A
  • not cancer like most other metaplasias

- instead, it is associated with fibrocystic change

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13
Q

What vitamin deficiency can result in metaplasia?

A

Vitamin A

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14
Q

What is Keratomalacia? What specific change does it involve?

A
  • a form of metaplasia arising from a vitamin deficiency
  • VitA is necessary for the differentiation of specialized epithelial surfaces
  • this is particularly true for the conjunctiva covering the eye
  • the thin squamous lining of the conjunctiva undergoes a change called keratomalacia to stratified keratinizing squamous epithelium
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15
Q

What is a classic example of mesenchymal connective tissue metaplasia?

A
  • myositis ossificans

- CT within muscle changes to bone during healing after trauma in part due to sustained inflammation

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16
Q

What is myositis ossificans?

A
  • a classic example of mesenchymal metaplasia

- CT within muscle changes to bone during the healing process after trauma thanks to sustained inflammation

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17
Q

At what point along the progression from hyperplasia and metaplasia to dysplasia to cancer, does the process become irreversible.

A
  • hyperplasia, metaplasia, and dysplasia are all reversible in theory
  • only a cancerous transformation is irreversible
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18
Q

What is aplasia?

A

a failure of cell production during embryogenesis

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19
Q

When does cellular injury occur?

A

when stress exceeds the cell’s ability to adapt (either in magnitude, duration, or rate of onset)

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20
Q

Neurons are highly susceptible to what kind of injury?

A

ischemic injury more than others

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21
Q

Through what mechanism does hypoxia lead to cellular injury?

A
  • oxygen is needed for energy production since it is the final electron acceptor
  • low oxygen delivery to tissue impairs oxidative phosphorylation and results in diminished ATP levels
  • low ATP disrupts key cellular functions such as Na/K-pump activity and calcium-pump activity
  • furthermore there is a switch to anaerobic glycolysis and the resulting build up of lactic acid denatures proteins and precipitates DNA
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22
Q

What is hypoxemia?

A

a cause of hypoxia in which there is a low partial pressure of oxygen in the blood (PaO2 <60 mmHg or SaO2 <90%)

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23
Q

List four causes of hypoxemia.

A
  • high altitude reduces FiO2 and affects PaO2
  • hypoventilation increases PACO2 and results in a decreased PAO2
  • a diffusion defect (e.g. interstitial pulmonary fibrosis), limits PaO2
  • a V/Q mismatch (e.g. right-to-left shunt or atelectasis) reduces PaO2
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24
Q

What are the two most significant causes of decreased O2-carrying capacity, which contribute to hypoxia?

A
  • anemia

- CO poisoning

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25
Q

CO Poisoning

A
  • CO binds hemoglobin more avidly than oxygen so while PaO2 is normal, SaO2 is diminished
  • this causes hypoxia and cellular injury
  • exposure usually comes from smoke or exhaust inhalation
  • classically, there is a cherry-red appearance of the skin and the most signficant sign of exposure is headache
  • ultimately it leads to coma and death
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26
Q

What is Methemoglobinemia?

A
  • a cause of hypoxia in which iron in heme is oxidized to the Fe3+ state, which cannot bind oxygen
  • usually due to oxidant stress (e.g. exposure to nitrites) or in newborns
  • classically presents with cyanosis and chocolate-colored blood
  • treatment is IV methylene blue which helps generate mediators of iron reduction
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27
Q

The hallmark of reversible cellular injury is what? How can this be identified?

A

cellular swelling, which results in loss of microvilli and membrane blabbing as well as dissociation of ribosomes from the swelling RER, which causes a decline in protein synthesis

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28
Q

The hallmarks fo reversible and irreversible cellular injury are what? What is the hallmark of cell death?

A
  • reversible: swelling
  • irreversible: membrane damage
  • death: loss of the nucleus
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29
Q

Irreversible cellular injury is defined by membrane damage. What does membrane damage result in and why is it irreversible?

A
  • plasma membrane damage causes cytosolic enzymes to leak into serum and additional calcium to enter the cell
  • mitochondrial membrane damage triggers a loss of the electron transport chain and leakage of cytochrome c into the cytosol
  • lysosome membrane damage result in hydrolytic enzymes leaking, where they are activated by the elevated intracellular calcium
  • mitochondrial membrane damage is the most significant because the loss of electron transport chain means even restoring O2 delivery can’t save the cell and cytochrome c release, induces apoptosis
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30
Q

Describe how hypoxia leads to irreversible cell injury.

A
  • hypoxia is low oxygen delivery to tissue
  • since oxygen is the final electron acceptor, it impairs oxidative phosphorylation and results in a lack of ATP
  • without ATP, the Na/K and Ca pumps stop working and there is a switch to anaerobic glycolysis
  • sodium, water, and calcium build up in the cell while lactic acid denatures proteins and precipitates DNa
  • the cell begins to swell (hallmark of reversible injury), which results in a loss of microvilli, dissociation of ribosomes from the RER, and membrane damage
  • membrane damage then marks irreversible injury
  • cytosolic enzymes leak into the serum while additional calcium enters the cell
  • lysosomal enzymes leak into the cytosol and are activated by the elevated calcium
  • mitochondrial membrane damage results in a loss of electron transport chain so that even if O2 delivery is restored, ATP production can’t continue
  • mitochondrial membrane damage also causes a leakage of cytochrome c, which induces apoptosis
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31
Q

The hallmark of cellular death is loss of the nucleus. Through what stages does this occur?

A
  • pyknosis = condensation
  • karyorrhexis = fragmentation
  • karyolysis = dissolution
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32
Q

What are the two mechanisms of cell death?

A

necrosis and apoptosis

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33
Q

What is necrosis?

A

death of large groups of cells followed by acute inflammation (neutrophil infiltrate) due to some underlying pathologic process

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34
Q

How does necrosis compare to apoptosis?

A
  • necrosis is the death of large groups of cells while apoptosis usually involves single cells or smaller groups
  • apoptosis, in contrast to necrosis, is an energy-dependent process
  • apoptosis can be physiologic whereas necrosis is always pathologic
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35
Q

What are the six types of necrosis?

A
  • coagulative
  • liquefactive
  • gangrenous
  • caseous
  • fat
  • fibrinoid
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36
Q

Describe coagulative necrosis? What is it typically characteristic of?

A
  • a form of necrosis in which the necrotic tissue remains firm and cell shape and organ structure are preserved while the nucleus disappears
  • typically characteristic of ischemic infarction of any organ except the brain
  • seen as a wedge-shaped area pointing to teh focus of vascular occlusion
  • a subset is red infarction, which arises if blood re-enters a loosely organized tissue (e.g. after a testicular torsion disrupts the vein causing necrosis but continues to be supplied by the artery)
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37
Q

What is red infarction?

A
  • a subset of coagulative necrosis (the other being pale infarction)
  • occurs when blood re-enters loosely organized necrotic tissue (i.e. tissues with multiple blood supplies)
  • for example, testicular torsion may collapse the vein without disrupting the artery so blood continues to flow in
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38
Q

Describe liquefactive necrosis. What is it characteristic of?

A
  • necrotic tissue that becomes liquefied due to enzymatic lysis of cells and proteins
  • characteristic of brain infarction, abscesses, and pancreatitis because of microglial enzymes, neutrophil enzymes, and pancreatic enzymes, respectively
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39
Q

Describe gangrenous necrosis? What is the difference between wet and dry gangrene? What is it characteristic of?

A
  • coagulative necrosis that resembles mummified tissue is called dry gangrene
  • if a superimposed infection of the dead tissue occurs, then liquefactive necrosis ensues and this is called wet gangrene
  • it is characteristic of chronic ischemia in the lower limb and GI tract, particularly in diabetics?
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40
Q

Describe caseous necrosis? What is it characteristic of?

A
  • consists of soft, friable necrotic tissue with a “cottage cheese-like” appearance
  • a combination of coagulative and liquefactive necrosis
  • characteristic of granulomatous inflammation due to TB or fungal infection
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41
Q

Describe fat necrosis and the mechanism that contributes to it. What is it characteristic of?

A
  • necrotic adipose tissue with a chalky-white appearance due to the deposition of calcium
  • calcium is deposited as fatty acids are released and bind calcium, a process called saponification
  • characteristic of trauma to fat and pancreatitis-mediated damage of peripancreatic fat
  • appears dark blue on histology
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42
Q

What is saponification?

A
  • an example of dystrophic calcification
  • the process whereby, free fatty acids bind calcium and precipitate as calcium deposits
  • a feature of fat necrosis
43
Q

Pancreatitis will lead to what kind(s) of necrosis?

A
  • the parenchyma will undergo liquefactive necrosis due to the presence of pancreatic enzymes
  • the peripancreatic fat undergoes fat necrosis as lipase is released and frees fatty acids
44
Q

What is the difference between dystrophic and metastatic calcification? Give examples of each.

A
  • dystrophic is calcification of abnormal tissue in the setting of normal serum calcium and phosphate levels (e.g. saponification of fat necrosis) and tends to be localized
  • metastatic calcification occurs when high serum calcium or phosphate levels lead to calcium deposition in normal tissue (e.g. hyperparathyroidism leading to nephrocalcinosis) and tends to be more widespread
45
Q

Describe fibrinoid necrosis. What two conditions is it highly characteristic of?

A
  • necrotic damage to the blood vessel wall
  • leaking of proteins like fibrin into the vessel wall result in bright pink, thick staining of the wall microscopically
  • characteristic of malignant hypertension (e.g. pre-eclapsia resulting in fibrinoid necrosis of the placenta) and vasculitis
46
Q

Give three examples of physiologic apoptosis.

A
  • endometrial shedding
  • removal of cells during embryogenesis
  • CD8 T cell-mediated killing of virally infected cells
47
Q

Describe the changes seen in a cell undergoing apoptosis.

A
  • the dying cell shrinks, leading the cytoplasm to become more eosinophilic while the nucleus condenses and fragments in an organized manner and is extremely basophilic
  • apoptotic bodies fall from the cell and are removed by macrophages
  • it is not followed by inflammation
48
Q

Apoptosis is mediated by what group of proteins? How do they function?

A

capsases, which activate proteases and endonucleases

49
Q

How is apoptosis triggered? In other words, how do caspases become activated?

A
  • intrinsic pathway: damage leads to inactivation of Bcl2; Bcl2 normally prevents cytochrome c release by binding and inhibiting APAF-1 and without it cytochrome c is free to activate caspase 9
  • extrinsic receptor-ligand pathway: FasL binds Fas or TNF binds the TNF receptor, activating caspases
  • cytotoxic CD8 T cell-mediated pathway: perforin create pores through which granzyme enters and activates caspases
50
Q

Which free radical is most damaging?

A

the hydroxyl radical

51
Q

How are free radicals generated physiologically?

A

during oxidative phosphorylation, partial reduction of O2 yields superoxide, hydrogen peroxide, and hydroxyl radicals

52
Q

Describe four mechanisms for the pathologic generation of ROS and the species they create.

A
  • ionizing radiation produces hydroxyl free radicals
  • inflammation generates superoxide ions during the oxidative burst
  • metals like iron and copper are normally bound, but when free they generate hydroxyl free radicals
  • drugs and chemicals are metabolized by the P450 system, generating free radicals
53
Q

The damage associated with Wilson’s disease and hemochromatosis is mediated by what?

A

the free radicals species produced by free copper or iron

54
Q

How do free radicals cause cellular injury?

A

they peroxidate lipids and oxidate DNA and proteins

55
Q

Which enzymes are responsible for the elimination of free radicals?

A
  • superoxide dismutase reduces superoxide to hydrogen peroxide
  • catalase reduces hydrogen peroxide to oxygen and water
  • glutathione peroxidase reduces primarily hydroxyl radicals by oxidizing two molecules of glutathione
56
Q

What is carbon tetrachloride? How does exposure manifest?

A
  • CCl4 an organic solvent used in the dry cleaning industry
  • P450 converts it to a CCl3 free radical
  • this results in hepatocyte injury, which in turn contributes to decreased apolipoprotein synthesis and fatty change in the liver
57
Q

What is reperfusion injury?

A
  • damage to tissue that follows restoration of blood for to an ischemic tissue
  • repefusion results in the formation of oxygen-derived free radicals
58
Q

An individual presents with an MI and is treated; however, his cardiac enzymes are continuing to rise. What is occurring?

A

he is experiencing a repercussion injury mediated by free radicals

59
Q

Define and describe amyloid. How can we identify it?

A
  • a misfolded protein that deposits in the extracellular space
  • typically has a beta-pleated sheet configuration
  • it is identified using Congo red stain which then demonstrates apple-green birefringence under polarized light
60
Q

Primary Systemic Amyloidosis

A
  • systemic deposition of AL amyloid, which is derived from immunoglobulin light chain
  • associated with plasma cell dyscrasias like multiple myeloma
61
Q

Secondary Systemic Amyloidosis

A
  • a systemic deposition of AA amyloid, which is derived from serum amyloid-associated protein, a positive acute phase reactant
  • levels increase during a chronic inflammatory state, malignancy, and Familial Mediterranean Fever
  • clinical findings depending on the tissue affect but the kidney is most commonly involved, producing a nephrotic syndrome, and the heart is often involved, producing a restrictive cardiomyopathy or arrhythmia
  • diagnosis requires a tissue biopsy and damaged organs must be transplanted
62
Q

Familial Mediterranean Fever

A
  • an autosomal recessive condition due to dysfunctional neutrophils
  • occurs in persons of Mediterranean origin
  • presents with episodes of fever and acute serial inflammation, which may mimic appendicitis, arthritis, or MI
  • SSA becomes elevated during the course, contributing to a secondary systemic amyloidosis (nephrotic syndrome and restrictive cardiomyopathy likely)
63
Q

Senile Cardiac Amyloidosis

A
  • non-mutated serum transthyretin deposits in the heart
  • usually asymptomatic
  • seen in more than 25% of people over 80 years old
64
Q

Familial Amyloid Cardiomyopathy

A
  • mutated serum transthyretin deposits in the heart
  • contributes to a restrictive cardiomyopathy
  • prevalent amongst African Americans
65
Q

Diabetes-Associated Amyloidosis

A
  • amylin, a derivative of insulin, is deposited in the islets of the pancreas
  • also known as islet amyloid polypeptide
66
Q

Dialysis-Associated Amyloidosis

A
  • B2-microglobulin (a structural support for MHC-I) deposits in the joints
  • may present as carpal tunnel syndrome
67
Q

Give six examples of localized amyloidosis and the protein that is deposited.

A
  • senile cardiac amyloidosis: non-mutated transthyretin
  • familial amyloid cardiomyopathy: mutated transthyretin
  • non-insulin-dependnent diabetes mellitus: amylin
  • Alzheimer disease: AB amyloid
  • Dialysis-Associated amyloidosis: B2-microglobulin
  • Medullary carcinoma of the hyoid: calcitonin
68
Q

Medullary Carcinoma of the Thyroid

A
  • a tumor derived form C-cells, which produce calcitonin
  • calcitonin deposits within the tumor, causing an amyloidosis
  • classically described as “tumor cells in an amyloid background”
69
Q

What is DNA laddering?

A

fragments in multiples of 180 bp that are a sensitive indicator of apoptosis

70
Q

What are the roles of Bcl-2, BAX, and BAK?

A
  • BAX and BAK are proapoptotic

- Bcl-2 inhibits APAF-1 and cytochrome release and is anti-apoptotic

71
Q

What kind of apoptosis mediates negative selection of T cells in the thymic medulla?

A

Fas-FasL (extrinsic death receptor pathway)

72
Q

Which regions of the brain, heart, kidney, liver, and colon are most susceptible to ischemic injury?

A
  • brain: ACA, MCA, PCA boundary areas
  • heart: subendocardium of the LV
  • kidney: straight segment of the proximal tubule and thick ascending limb
  • liver: zone III (around the central vein)
  • colon: splenic flexure and rectum
73
Q

What are watershed zones?

A
  • areas that receive blood supply from the most distal branches of two arteries with limited collateral vascularity, leaving them highly susceptible to hypo perfusion ischemia
  • primary examples are in the brain and at the splenic flexure and rectum in the GI tract
74
Q

Which neurons in the brain are most vulnerable to hypoxic-ischemic insult?

A
  • Purkinje cells of the cerebellum
  • pyramidal cells of the hippocampus
  • neocrotex
75
Q

In which organs does metastatic calcification tend to predominate? Why?

A
  • interstitial tissues of the kidney, lung, and gastric mucosa are most affected
  • this is because these tissues lose acid quickly and a basic pH favors deposition
76
Q

Describe inhalation injury (causes, presentation, sequelae)

A
  • a pulmonary complication associated with smoke and fire
  • caused by heat, microscopic particles, or irritants
  • leads to chemical tracheobronchitis, edema, pneumonia, and ARDS
  • many patients present secondary to buns, CO inhalation, or arsenic poisoning
77
Q

Describe lipofuscin. What is it indicative of? How does it form?

A
  • it is a yellow-brown pigment associated with normal aging
  • it is associated with “wear and tear”
  • formed by oxidation and polymerization of autophagocytosed organelle membranes
78
Q

Chromatolysis

A
  • a histologic reaction of neuronal cell body to axonal injury
  • the changes reflect increased protein synthesis as the cell attempts to repair a damaged axon
  • the cell swells and rounds, the nucleus is displaced to the periphery, and Nissl substance disperses throughout the cytoplasm
  • accompanies Wallerian degeneration (degeneration of axon distal to site of injury)
79
Q

Hyperacute Rejection

A
  • a type II hypersensitivity that occurs within minutes
  • mediated by preformed recipient antibodies against donor antigens
  • leads to widespread necrosis of graft vessels and thus ischemia and necrosis of the transplant
  • requires graft removal
80
Q

Acute Rejection

A
  • a type IV hypersensitivity that occurs in weeks to months
  • there is a cellular (CD4 and CD8) and a humoral component
  • causes vasculitis with a dense lymphocytic interstitial infiltrate
  • this is what immunosuppression is used to prevent
81
Q

Chronic Rejection

A
  • a type II and IV hypersensitivity in months to years
  • mediated by CD4 cells responding to donor peptides being presented on recipient MHCs
  • results in proliferation of vascular smooth muscle, parenchymal atrophy, and interstitial fibrosis
82
Q

GvHD

A
  • most common in bone marrow and liver transplants
  • due to engrafted T cells attacking donor antigens, making it a type IV hypersensitivity
  • presents with a maculopapular rash, hepatosplenomegaly, jaundice, and diarrhea
83
Q

What is the difference between type I, II, and IV renal tubular acidosis?

A
  • type I: due to inability of a-intercalated cells to secrete protons, so no new bicarb is produced; urine pH > 5.5; serum potassium low
  • type II: due to inability of PCT to adequately reabsorb bicarb; urine pH < 5.5 because a-intercalated cells attempt to compensate; serum potassium low
  • type IV: due to hypoaldosteronism or aldosterone resistance; urine pH < 5.5; serum potassium high
84
Q

What would cause a type I, II, or IV renal tubular acidosis?

A
  • type I: amphotericin B toxicity, analgesic nephropathy, congenital anomalies of the urinary tract, SLE
  • type II: fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors
  • type IV: low aldosterone or aldosterone resistance
85
Q

Trisomy 21

A
  • caused by meiotic non-dysjunction due to maternal age, unbalanced Robertsonian translocation, or mitotic non-dysfunction
  • presents with nuchal translucency and hypoplasia of the nasal bone on ultrasound in the first trimester
  • amniotic fluid in the first trimester demonstrates elevated B-hCG and diminished PPAP-A
  • amniotic fluid in the second trimester demonstrates low AFP, elevated B-hCG, low estriol, and elevated inhibin A
  • presents with intellectual disability, risk for Alzheimer’s, duodenal atresia, Hirschsprung disease, risk of ALL or AML, prominent epicanthal folds, Brushfield spots, and AV septal defects
86
Q

Trisomy 18

A
  • the second most common cause of trisomy, known as Edward’s syndrome
  • in utero, B-hCG and PPAP-A are low in the first trimester; AFP, B-hCG, estriol, and inhibin A are low in the second
  • findings described by “PRINCE Edward”: prominent occiput, rocker bottom feet, intellectual disability, nondisjunction, clenched fists with overlapping fingers, low-set ears
  • plus micrognathia and congenital heart disease
87
Q

Trisomy 13

A
  • known as Patau syndrome
  • B-hCG and PPAP-A are low in the first trimester
  • microcephaly, holoprosencephaly, intellectual disability
  • microphthalmia, cleft lip/palate
  • congenital heart disease
  • PKD
  • cutis aplasia, polydactyly, rocker bottom feet
88
Q

What is the mechanism of action for tacrolimus?

A

it forms a complex with FKBP and inhibits calcineurin, preventing activation of NFAT, which is a pro-inflammatory transcription factor

89
Q

What is the mechanism of action for cyclosporine?

A

it forms a complex with cyclophilin and inhibits calcineurin, preventing activation of NFAT, which is a pro-inflammatory transcription factor

90
Q

What is the mechanism of action for sirolimus?

A

it forms a complex with FKBP and inhibits mTOR, a protein in the IL-2R signal cascade, which stimulates cell proliferation

91
Q

Name two monoclonal antibodies that inhibit IL-2R.

A

daclizumab and basiliximab

92
Q

How do tacrolimus, cyclosporine, and sirolimus compare in regards to toxicity?

A
  • tacrolimus is most nephrotoxic
  • cyclosporine is nephrotoxic
  • sirolimus is not nephrotoxic (the kidneys “sir”vives)
93
Q

What are the effects of dopamine, somatostatin, TRH, and CRH in the hypothalamic-pituitary axis?

A
  • dopamine inhibits release of prolactin and TSH
  • TRH promotes the release of prolactin and TSH
  • somatostatin inhibits the release of GH and TSH
  • CRH promotes the release of ACTH, MSH, and B-endorphin
94
Q

Phenylalanine is a precursor for what?

A
  • tyrosine
  • thyroxin
  • catecholamines
  • melanin
95
Q

Tryptophan is a precursor for what?

A
  • serotonin and melatonin (requires B6/pyridoxine and BH4)

- niacin, NAD, and NADP (requires B2 and B6/pyridoxine)

96
Q

Glycine is a precursor for what?

A

porphyrin

97
Q

Glutamate is a precursor for what?

A

GABA and glutathione

98
Q

Argining is a precursor for what?

A

NO, urea, and creatine

99
Q

Describe proper verbal development.

A
  • oratory by 10 months
  • 200 words by age 2 with 2 word phrases
  • 1000 words by age 3 with complete sentences
  • full stories by age 4
100
Q

Describe proper motor development.

A
  • rolls and sits by 6 months
  • crawls by 8 months
  • stands by 10 months
  • first steps by 12 months
  • kicks ball by 24 months
  • drives tricycle by 3 years
  • copies lines and circles by 4 years
  • hops on one foot by 4 years
  • grooms and dresses by 5 years
101
Q

What cartilage and nerves arise from branchial arches 1, 2, 3, and 4/6?

A
  • 1: maxillary, mandible, malleus and incus plus CN V3
  • 2: stapes, and lesser horn of hyoid plus CN VII
  • 3: greater horn of hyoid plus CN IX
  • 4/6: cricoid plus CN X
102
Q

What are the derivatives of the 1st, 2nd, 3rd, and 4th branchial pouches?

A
  • 1: eustachian
  • 2: epithelial lining of palatine tonsils
  • 3: inferior parathyroid and thymus
  • 4: superior parathyroid and parafollicular C cells of thyroid
103
Q

List the important CYP inducers.

A
  • carbamazepine
  • cyclophosphamide
  • griseofulvin
  • modafinil
  • phenytoin
  • rifampin
  • St. John’s wort
104
Q

List the important CYP inhibitors.

A
  • Amiodarone
  • Azoles
  • Clarithromycin
  • Cimetidine
  • Fluoroquinolones
  • Grape Fruit Juice
  • Isoniazid
  • Ritonavir

STEP1 (24 decks)

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