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From Flashcardlet > 5/8 > Flashcards

5/8 Flashcards

1
Q

What nitrate has 100% bioavaliability when given orally?

What nitrate is IV and used for HTN emergency?

What nitrate is put under the tongue?

A

Isosorbide mononitrate - it is the only oral drug that has 100% bioavaliability

IV = sodium nitroprusside

under tongue = nitroglycerin

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2
Q

Are cox-1 and cox-2 normally present in tissues?

A

Cox-1 is, cox-2 is only present at times of inflammation

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3
Q

What eating condition found during pregnancy is associated with iron deficiency?

A

PICA - you eat strange stuff and have a tendency to crave ice (iron def)

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4
Q

Where is a pulmonary emboli most likely originating from? Where is a renal emboli coming from?

A

Pulm = deep vein thrombosis

Renal = Left side of the heart/aorta

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5
Q

What enzyme can be used as a marker for mast cell degranulation?

A

Tryptase

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6
Q

What is 5-hydroxyindoleacetic acid and what disease is the breakdown diagnostic for?

A

5-HT = breakdown product of serotonin. It can be used to screen for carcinoid tumors (excess serotonin)

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7
Q

Where is K+ reabsorbed in the nephron tubules?

Where is it secreted?

A

65% reabsorbed in the PCT and the other 35% in the Ascending loop (due to Na/K/Cl channels

It is secreted back into the tubule (regulated) by principle cells in the CT

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8
Q

What is the main cause of homocyteinuria?

What enzymes and cofactors are involved here?

What is the end product?

A

Main cause = cystathionine synthetase def. = Homocysteine cant be converted to cystathionine. This step also requires B6 and Serine.

The end product in this pathway is the production of cysteine from cystathionine via the enzyme Cystathionase (B6 needed here too)

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9
Q

What is the folate trap? What causes this?
What products are not made?

What dz does this cause?

A

The folate trap is when 5-Methyl THF cant get turned back into THF (catalyzed by methionine synthase)

This is mainly due to B12 (cobalamin) deficiency, as it is made into methylcobalamin while being used to make THF

As a result, homocysteine builds up (detected in the urine) and Methionine and THF are not made.

This results in a megaloblastic anemia and homocysteinurea

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10
Q

What are the ergot and nonergot dopamine agonists?

A

ergot = bromocriptine and pergolide

nonergot = pramipexole and ropinirole

These seek D2 receptors and do NOT have to be metabolized to work. They treat parkinsons. Bromo can also treat a prolactinoma

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11
Q

What is the phenomena responsible for a pt awakening 30 min after thiopental was given to induce anesthetic?

A

Redistribution

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12
Q

What are the MOAs of mifepristone and misoprostol?

A

Mifepristone = anti-progestin used to induce abortions

Misoprostil = PGE agonist used to induce contractions

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13
Q

What is Ribaviran used for? What is its MOA?

A

Ribaviran treats HCV by acting as a guanine analog and blocking RNA polymerase

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14
Q

What is calcineurin?

A

It is a protein phosphatase in T cells that can activate IL-2 secretion thus supporting T cell growth and development

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15
Q

What is a shilling test?

A

The administration of IF to determine the cause of abnormal B12 absorption. If B12 levels rise (+ test) then the pt has pernicious anemia

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16
Q

What do HAV and HEV have in common, who is at an increased risk for HEV?

A

They are both fecal-oral transmitted. HEV is common in pregnant women

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17
Q

How do HBV and HCV differ?

A 
HBV = sexual transmission, can turn chronic. Tx = vaccine or a-interferon
HCV = IV drug use, can turn chronic. Tx = a-interferon+ribaviron
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18
Q

What do each of the HBV serology markers represent?

A 
HBsAg: indicates current HBV infection
HBs-Ab: indicates immunity to HBV
HBeAg: indicates high transmissability
HBe-Ab: indicates low transmissability 
HBcAg: indicates a new infection
HBc-Ab: indicates prior exposure, + during window period

Don’t see HBc-Ab in vaccinated ppl, but will see HBs-Ab

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19
Q

How is Leishmania Donovani transmitted? What dz does it cause

What are the histological findings?

Tx?

A

Sandfly bit –> spiking fevers w/ hepatosplenomegaly and a pancytopenia. Can get hand/face papules if you get the cutaneous kind.

Histo = macrophages w/ amastigotes inside
Tx: Na- Stibogluconate

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20
Q

How is Entamoeba Histolytica transmitted? What dz does it cause?

What are the histological findings?

Tx?

A

Cysts in infected water –> amebiasis (bloody diarrhea) with liver abscess w/ anchovy past exudate. If this liver abscess ruptures you are left with a flask shaped ulcer

Histo = Trophozoites w/ RBCs in the cytoplasm or poo with multinuclei.

Tx: Metro

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21
Q

What is the classic triad in hemochromatosis? What risks does this dz lead to?

How do you get the dz?

What will labs look like?

Tx?

A 
Triad = cirrhosis, DM, bronze skin due to increased hemosiderin in the skin causing free rad damage
Risks = CHF, teste atrophy, liver CA
Patho = AR inheritance or multiple blood infusions (sickle cell/B-thal)

Labs = increased ferritin, transferrin saturation, and iron, decreased TIBC

Tx: Deferoxamine

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22
Q

What Abs will be present in autoimmune hepatitis?

A

Anti-ANA, Smooth muscle, and liver-kidney microsomal Abs

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23
Q

How is a-1 antitrypsin genetically inherited?

What clinical signs?

A

Codominant trait

Lungs = decreased elastic tissue (thx to elastase) with a panacinar emphysema

Liver = cirrhosis w/ PAS+ globules

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24
Q

What are the main risk factors for Hepatic Adenoma and Angiosarcoma?

A

HA = OCP use and type 1 and 3 glycogen storage diseases

Angio = exposure to arsenic or polyvinyl chloride

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25
Q

How can aspergillus lead to hepatocellular carcinoma?

What marker is used to dx the CA?

A

Aspergillus = increased aflatoxin –> increase p53 mutations

AFP

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26
Q

How do you aquire a clonorhis sinensis infection? What dz can it lead to and what is the tx?

A

Eating undercooked fish, this is a fluke

Can lead to biliary tract inflammation, pigmented gallstones or cholangiocarcinoma

Tx: Praziquantel

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27
Q

What are the potentials for an unconjugated hyperbilirubinemia?

A

increased bili production: hemolytic anemia, sickle cell, hematoma breakdown

impaired bili uptake/storage: post viral hepatitis, rifampin use

decreased UDP-GT: Gilberts, Criglar Najjars, Neonatal jaundice

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28
Q

What are the potentials for conjugated hyperbilirubinemia?

A

Impaired transport: Dubin Johnson, Roters

Intrahepatic biliary obstruction: 1* Biliary Cirrhosis, 1* Sclerosing Cholangitis, Chlorpromazine and Arsenic

Extrahepatic biliary obstruction: pancreatic CA, Choledocholithias, pancreatitis, cholangiocarcinoma

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29
Q

What is Primary Sclerosing Cholangitis, what are diagnostic criteria?

A

An idiopathic concentric “onion-skinning” “florrid duct” fibrosis of the bile duct w/ beaded appearance.

Associated with U.C. +P-ANCA and has a risk for cholangiocarcinoma

30
Q

What is Primary Biliary Cirrhosis, what are the diagnostic criteria?

A

An autoimmune rxn w/ lymphocytic infiltrate and granulomas.

Pt will be a woman w/ other autoimmune disorders and pruritis w/o jaundice. +AMA

Tx: Ursodiol (decreases liver synth of cholesterol which leads to less in stones)

31
Q

Secondary Biliary Cirrhosis

A

Due to extrahepatic biliary obstruction –> increased pressure in intrahepatic ducts –> fibrosis and bile stasis

Clx: pruritis, jaundice, dark urine, and increased alk phos

32
Q

Cholelithiasis, Cholecystitis, Cholangitis, Choledocholithiasis

A

Cholelithiasis: gallstones
Cholecystitis: inflammation/infection of gallbladder
Cholangitis: inflammaion of biliary tree
Choledocholithiasis: gallstones in the bile ducts

33
Q

What are the main causes of yellow, black stones and brown gallstones?

A

Yellow/Radiolucent = cholesterol stones; FFFF, estrogens, clofibrate (hmg CoA blocker)

Black = hemolysis

Brown = infection

34
Q

What is biliary colic, what is one tx?

A

When a gallstone is pushed from the gallbladder into the biliary tree in response to CCK. Can present w/o pain in a diabetic!

Tx: Dicyclomine: anti-cholinergic SM relaxer which can decrease the pain of colic

35
Q

What is Reynolds pentad for cholangitis?

A

Charcots triad (fever, jaundice, and RUQ pain) + hypotension, and altered mental status.

All gallbladder problems will be associated with increased alk phos

36
Q

What are some good supplements for Omega 3 FAs?

A

Eicosapentaenoic Acid (EPA)

Docosahexaenoic Acid (DHA)

a-Linolenic acid (ALA)

37
Q

What is the key to refeeding a starving person? Why?

A

Go slow, use milk

refeeding syndrome can occur if glucose is given to a starving person. This is b/c the starved cells absorb so much glucose they also take K and P and Mg and Ca and the body is now at risk for arrythmias.

Also a huge decrease of ATP b/c the cell takes in a ton of phospherous and holds it to trap all the nutrients into the cell

38
Q

What change is seen to RBCs of Abetalipoproteinemia pts?

A

Acanthocytosis: mace shaped spiking of RBCs

39
Q

What role do Apo E, AII, CII, B48, and B100 have?

A 
E: mediates uptake of remnant particles
AII: activates LCAT
CII: Cofactor for LPL
B48: Mediates chylomicron secretion
B100: Binds LDL receptor
40
Q

What are the clinical manifestations of a CAT (carnitine shuttle) def?

A

Inability to transport LCFAs into the mitochondria for breakdown via beta ox to energy = weakness, hypotonia, and hypoketotic hypoglycemia

41
Q

What are the functions of Chylomicrons, VLDLs, IDLs, LDLs, and HDLs?

A

Chylo: transports TGs to peripheral tissues and transports cholesterol to the liver (secreted by GI cells)
VLDL: delivers hepatic TGs to peripheral tissues
IDL: formed from degradation of VLDLs –> delivers TGs and cholesterol to liver
LDL: delivers cholesterol from liver to peripheral tissues. Taken up by target cells via receptor mediated endocytosis (clathrin coated pits)
HDL: reverse cholesterol transport from periphery to liver. Repository for apoC and E (secreted from liver and GI)

42
Q

What is the drug cocktail used to treat severe cirrhosis?

A

Vitamin K: increase clotting
Lactulose: creates acidic colon and draws ammonia out of body trapping it as ammonium
Diuretics
B-Blockers (nadalol, propranalol) to decrease bleeding varices

43
Q

What important NTs does phenylalanine turn into?

What does carbidopa do?

A

Phe –> Tyrosine –> Tyroxine (thyroid hormone) and Dopa

Dopa –> Melanin and Dopamine (Carbidopa blocks dopa to dopamine conversion by dopa decarboxylase)

Dopa –> Ne –> Epi

44
Q

What important NTs does Tryptophan turn into?

A

Niacin (w/ B6) and Serotonin

45
Q

What NTs do histidine and glycine turn into?

Arginine?

Glutamate?

A

Histamine

Glycine –> Porphyrin (w/ B6) –> Heme

Arginine –> Creatine, Urea, NO

Glutamate –> GABA and Glutathione

46
Q

What does an elevated or decreased BUN mean?

A

elevated = urea cycle is making urea but it is not leaving the body.

Decreased = urea cycle is not working (possibly an OTC def)

47
Q

What is the clinical manifestation of an OTC (urea cycle def?)

Tx?

A

X-linked R

Presents 2 weeks after birth as an alkalotic baby w/ cerebral edema (Hepatoencephalopathy)

Tx: Phenylbutyrate (binds and excretes AAs)

48
Q

What does dopamine, NE, and Epi break down into?

A 
Dopamine = HVA
NE = VMA
Epi = Metanephrine
49
Q

PKU & Maternal PKU

A

def: phenylalanine hydroxylase OR BH4 –> phe build up and no tyrosine.
clx: musty smell, MR, siezures, fair skin
dx: test phenylketone levels in blood 2-3 days after birth (must give time for moms enzyme to wash away to get a true read.)
tx: no aspartame, supp tyrosine

Maternal PKU: mom decides to drink diet coke while pregnant even though she is pKU = teratogenic –> baby gets microcephaly, MR, and heart defects

50
Q

Alkaptonuria

A

def: homogentisic acid oxidase –> tyrosine is not degraded to fumarate correctly
clx: brown pigment in joints and eyes, joint pain, black pee

51
Q

Albinism

A

def: AR tyrosinase (cant convert tyrosine to melanin) or Defective tyrosine transporters (decreased amount of tyrosine). Can also be due to lack of migration of neural crest cells

Locus heterogeneity - so variable inheritance

52
Q

Homocystinuria

A

def: Cystathione synthase = tx with low methionine, hi cysteine, b12 and folate
def: decreased affinity of Cys synthase for B6 = tx with B6
def: homocysteine methyltransferase = tx with B12

All forms have homocysteinuria, MR, downward lens subluxation (marfans is up)

53
Q

Cystinuria

A

def: (AR) COLA transporter in PCT (cysteine, ornithine, lysine, and arginine)
clx: renal staghorn calculi and hexagonal crystals

Tx: hydration and urinary alkylation

54
Q

Hartnup Disease

A

def: (AR) neutral amino acid transporter on renal and GI cells –> too much tryptophan excretion in urine and low absorption in gut

Clx: Pellagra (niacin def) = dementia, dermatitis, diarrhea, DEATH

55
Q

What are some p450 inhibitors?

A 
PICK EGS:
P.I.s
Isoniazid
Cimetidine
Ketoconazole
Erythromycin
GF juice
Sulfonamides
56
Q

What are some p450 Inducers?

A

BCG PQRS:

Barbs
Carbamazepine
Griseofulvin
Phenytoin
Quinidine
Rifampin
St. Johns Wart
57
Q

What does the pKa represent?

How would you treat an acidic drug OD? Basic?

A

pKa = pH when the amount of non-protonated form of a drug (A- or B) is equal to the protonated form (HA or BH+)

acidic drug OD = trap it in a basic urine (protonated form of drug) - give NaHCO3

basic drug OD = trap it in an acidic urine - give NH4Cl

58
Q

Compare zero order vs first order elimination

A

Zero = PEA (phenytoin, ethanol, aspirin at high doses)
constant amount of drug is eliminated per unit time

1st order = rate of elimination is directly proportional to drug concentration (a constant fraction of drug is eliminated per time)

59
Q

What are some examples of acidic drugs?

Basic drugs?

A

acidic = aspirin, MTX, pehobarbitol (tx with bicarb)

basic = amphetamines (tx with ammonium chloride)

60
Q

Phase 1 vs Phase 2 drug metabolism

A

Phase 1 = responsible for oxidizing and hydrolysis via P450 –> yields slightly polar, water soluble, likely active drugs

Phase 2: GAS - glucuronidation, acetylation, and sulfation) –> yields very polar, inactive metabolite that is excreted in the urine

Old ppl lose phase 1 first

61
Q

What are B-blockers effect on renin?

A

B-blockers decrease renin levels via blocking B1 receptors on JG cells

62
Q

What portion of the kidney does the mesoderm and the uretic bud turn into?

A

uretic bud: collecting tubules and ducts, major and minor calyces, renal pelvis and the ureters

mesoderm: glomeruli, bowmans space, proximal tubules, loop of henle, and distal convoluted tubules

63
Q

Tuberous Sclerosis

A

(AD) cortical tubers w/ angiomyolipomas (fatty, SM kidney tumors) and subependymal hamartomas in the brain, seizures, MR, facial angiofibromas, leaf-shaped pigment-lacking patches on skin

64
Q

High potency vs low potency anti-psychotics? Examples of each?

A

low potency - chlorpromazine, thioridazine; side effects are sedation, anticholinergic, and orthostatic hypotension (H, ACh, and a1)

High Potency = Haloperidol, Fluphenazine; EPS (dystonia, akathisia, parkinsons

65
Q

What is the mode of action, common symptoms, and exam findings for phencyclidine, cocaine, and methamphetamine?

A

Phen: hallucinogen; will show hallucinations and violence; labs show nystagmus, and ataxia

Cocaine: Stimulant; will show euphoria, chest pain, siezures; labs show mydriasis

Meth: Stimulant; psychosis, sweating, violence; labs show tooth decay, HTN, choreiform movements

66
Q

What is the mode of action, common symptoms, and exam findings for LSD, marijuana, and heroin?

A

LSD: hallucinogen; hallucinations, euphoria, panic; labs show alert and oriented

Pot: Psychoactive drug; increased appetite, euphoria; dry mouth, conjuctival injection

Heroin: Opioid Analgesic; euphoria, coma; labs show miosis, decreased respiratory rate, decreased bowel sounds

67
Q

How does fetal Hb bind O2 so tightly?

A

It is unable to interact with 2,3 DPG (curve shifted to the left)

68
Q

What is the most sensitive test for diagnosing an incipient diabetic nephropathy?

A

Microalbuminuria test

69
Q

What is the MOA of nitroglycerin?

A

It decreases cardiac workload b/c it mainly works on venous system. Blood collects in the venous system (redistribution) and thus decreases preload –> decreases ventricular wall stress and thus decreasing cardiac o2 demand

70
Q

What do you use to treat p. aeruginosa and b. frag? (GnRs)

A

Piperacillin-tazobactam

71
Q

How does desmopressin (DDAVP) treat Von Willebrand disease?

A

Induces endothelial procoagulatory protein release (vWF). It does NOT act on V1 receptors (vasoconstriction)

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