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review / wrong answers > 3/25 - UWorld > Flashcards

3/25 - UWorld Flashcards

1
Q

In endometrial hyperplasia, is the more hyperplasia of the glands or the stroma?

A

glands

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2
Q

What is the cause of endometrial hyperplasia?

A

Unopposed estrogen

Often occurs in post-menopausal women when there is not progesterone to stop the bleeding caused by estrogen

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3
Q

What is the linea alba, and what defect can it cause

A

Linea alba is a mildine band of fibrous tissue that usually closes off the umbilical ring

Incomplete closure can lead to umbilical hernia

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4
Q

What is the difference between an omphalocele and gastroschisis

A

Both are caused when, during development, abd contents undergo herniation followed by rotation of midgut; but then there is failure of gut to return to abd cavity

Omphalocele - midline herniation of abd contents within a sac

Gastroschisis - full thickness abd wall defect with fully exposed abd contents

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5
Q

Which inguinal hernia goes through both the deep (internal) inguinal ring AND superficial (external) ring

A

Indirect inguinal hernia

INdirect also goes through INternal (deep) ring

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6
Q

Which inguinal hernia is a result of failure of processus vaginalis to close?

A

Indirect inguinal hernia

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7
Q

Which inguinal hernia occurs medial to the inferior epigastric vessel?

A

Direct inguinal hernia

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8
Q

Which inguinal hernia is covered by all 3 layers of spermatic fascia?

A

Indirect inguinal hernia (follows the descent of the testes)

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9
Q

How do corticosteroids lead to neutrophilia (increased neutrophils)

A

Demargination of neutrophils leads to increased neutrophil count (even though neutrophils ability to fight infection is decreased)

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10
Q

What enzyme does Aspirin act on? Reversible for irreversible?

A

COX-1 and COX-2

Irreversibly inhibits via acetylation

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11
Q

What enzyme does Acetaminophen work on? Reversible or irreversible?

A

Reversibly inhibits COX enzymes

Acts mostly in the CNS so can be used as an analgesic but not anti-inflammatory (weak in the periphery)

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12
Q

What enzyme does glucocorticoids work on?

A

Inhibition of phospholipase A2 (preventing production of AA)

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13
Q

What is the mechanism of acton of Celecoxib

A

It is a selective COX-2 inhibitor

Provides anti-inflammatory effects without effecting platelet function (lower risk of bleeding)

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14
Q

What enzyme do NSAIDs work on? Reversible or irreversible?

A

Reversibly inhibit both COX-1 and COX-2

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15
Q

Where in the cell does fatty acid synthesis occur?

A

Cytoplasm

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16
Q

Where is the cell does breakdown of fatty acids occur?

A

Mitochondria

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17
Q

What is the mechanism that allows fatty acids from the cytosol to be transported to the mitochondria for breakdown?

A

Carnitine shuttle (needed because negatively charged fatty acids cannot cross the plasma membrane)

Carnitine acyl transferease

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18
Q

What molecule inhibits carnitine acyle transferase?

A

Malonyl CoA

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19
Q

What are the ToRCHeS infections?

A 
Toxoplasmosis
Rubella
CMV
HIV/HSV
Syphilis
20
Q

Where is the most common location of H. Pylori colonization

A

Antrum of the stomach (where there are the least amount of acid-secreting parietal cells)

Even if ulcers are in the duodenum, H. Pylori can only colonize areas of gastric metaplasia

21
Q

Where is Secretin secreted from and what is it’s function?

A

Secreted from S cells of the duodenum in response to acidic chyme from the stomach

Stimulates pancreatic HCO3- secretion

22
Q

Where is VIP produced and what is its function?

A

VIP is produced in the pancreas and stimulates intestinal water secretion, counteracts gastrin in the stomach, and promotes bicarb secretion from the pancreas

23
Q

What are the symptoms of a VIPoma

A

WDHA syndrome:

Watery diarrhea, hypokalemia, achlorhydria

24
Q

Do you get a respiratory or metabolic acidosis in DKA and why?

A

Metabolic

No insulin –> no glucose inside cells and no inhibition of fatty acid breakdown –> fatty acids break down to acidic ketone bodies –> bicarb binds to ketonic bodies to try to neutralize –> metabolic acidosis

25
Q

What are the 3 methods that kidneys try to correct metabolic acidosis in DKA?

A

(1) Increased HCO3- reabsorption
(2) Increased H+ secretion (via H+ ATPase in the proximal tubule and alpha-interalated cells in the collecting duct)
(3) Increased acid buffer excretion (kidney uses acid buffers to trap H+ in the lumen to be excreted) - acid buffers include H(PO4)2- and NH3

26
Q

What nerve innervates the posterior external auditory canal

A

Small auricular branch of the vagus nerve

27
Q

What cranial nerve innervates most of the auditory canal (including the external portion of the TM)

A

Mandibular division of the trigeminal nerve (CN V3)

28
Q

What immune defense is responsible for protection against superficial candida infections?

A

T-cells

29
Q

What immune defense is responsible for protection against hematogenous Candidemia

A

Neutrophils

30
Q

What is the enzyme involved in the formation of pigmented gallstones?

A

Beta-glucuronidase

Bacterial infection (E. Coli) or heminthic infection (e.g Ascaris lumbricoides, Clonorchis sinensis) of the biliary tract leads to release of beta-glucuronidase by injured hepatocytes and bacteria

This enzyme hydrolyzes bilirubin glucuronides and increases the amount of unconjugated bilirubin

31
Q

Does histone acetylation lead to increased or decreased (silenced) gene expression?

A

Increased gene expression

Acetylation weakens the DNA-histone bond and makes DNA segments more accessible for transcription

32
Q

Does DNA methylation lead to increased or decreased gene expression?

A

Methylation inhibits gene transcription

Hypermethylation of the promoter region leads to transcriptional silencing

33
Q

Most common causes of neonatal meningitis

A

Group B strep, E. Coli, Listeria

34
Q

Most common causes of meningitis in older kids and adults

A

Strep pneumonia and Neisseria meningitidis and H. flu

35
Q

E. Coli virulence factor responsible for bacteriemia and septic shock

A

LPS

36
Q

E. coli virulence factor responsible for neonatal meningitis

A

K1 capsular polysaccharid

37
Q

E. Coli virulence factor responsible for bloody gastroenteritis

A

Verotoxin (Shiga-like toxin)

38
Q

E. coli virulence factor responsible for watery gastroenteritis

A

Heat labile enterotoxin (increases cAMP - eL Agua)

Heat stabile enterotoxin (increases cGMP - San Gabriel)

39
Q

E. Coli virulence factor responsible for UTI

A

fimbriae

40
Q

How do Enterococcus develop resistance to Aminoglycosides?

A

Inactivation of drug via acetylation enzyme

41
Q

Withdrawal symptoms:

Tremor, agitation, anxiety, delirium, psychosis, seizures, tachycardia, palpitations

A

Alcohol

42
Q

Withdrawal symptoms: Tremors, anxiety, perceptual disturbances, psychosis, insomnia, seizures, tachycardia, palitations

A

Benzodiazepines

43
Q

Withdrawal symptoms:

nausea, vomiting, abd cramping, muscle aches, dilated pupils, yawning, lacrimation

A

Heroin

44
Q

Withdrawal symptoms: increased appetite, hypersomnia, intense psychomotor retardation, depression

A

Stimulants (cocaine, amphetamines)

45
Q

Withdrawal symptoms: Dysphoria, irritibility, anxiety, increased appetite

A

Nicotine

46
Q

What is the attributable risk percent and what is the formula

A

ARP represents the excess risk in an exposed population that can be explained by exposure to a particular risk factor

ARP = 100 x [(risk in exposed - risk in unexposed) / risk in exposed]

47
Q

Describe the mechanism behind hepatic encephalopathy

A

Recall normal: Astrocytes take up glutamate (preventing excess neuronal excitation) and convert it to glutamine by combining with ammonia via glutamine sythetase; glutamine is then release to neurons where it can be converted back to glutamate to be used as an NT

In hepatic encephalopathy, there is too much ammonia which crosses the BBB and taken up by astrocytes, increasing glutamine production, therefore increasing intracellular osmolality and causing swelling of astrocyte and decreased glutamine release, leading to disruption of excitatory NT

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