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From Flashcardlet > 5/9 > Flashcards

5/9 Flashcards

1
Q

How does pulmonary edema affect lung compliance?

A

decreases lung compliance

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2
Q

validity = accuracy

precision = reliability

increased accuracy is the target, it is the trueness of test measurements

A

DONT FUCK THIS UP

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3
Q

What anticholinergic medication can be used to treat bradycardia? What is one possible side effect?

A

Atropine can be used to decrease vagal influences on SA and AV nodes.

Sdx: increased intraocular pressure –> glaucoma

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4
Q

What are symptoms of post-strep glomerulonephritis?

What kind of hypersensitivity is this?

A

edema, hematuria, hx of recent impetigo, or other strep infection,

Type III hypersensitivity = immune complexes deposited in the kidney

Glomerulous will have “lumpy-bumpy” look w/ humps

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5
Q

Be able to explain the 3 positive humps and 2 negative humps on the jugular venous pulse graph

A

a: (+) - RA contraction
c: (+) - bulge of tricuspid valve during RV contraction
x: (-) - atrial relaxation
v: (+) - continued inflow of new venous blood
y: (-) - passive RA emptying after tricuspid is open

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6
Q

What nerve is damaged in a + Trendelenburg test?

A

superior gluteal

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7
Q

Poorly soluble anesthetic vs highly soluble anesthetic

A

Poorly: (N2O) blood saturates fast and leads to a fast rise in partial pressure –> reaches the brain faster = LOW blood/gas partition coefficient

Highly: (Halothane) blood saturates slowly –> takes longer to reach the brain = HIGH blood/gas partition coefficient

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8
Q

What is the Inx, MOA, and Sdx for Bupropion?

A

Inx: drepression, tobacco dep

MOA: inhibits presynaptic reuptake of DA>NE

Sdx: Seizures

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9
Q

What does the enzyme 7a-hydroxylase do? What drugs inhibit this and what are the effects?

A

converts cholesterol to bile acids

Fibrates inhibit this enzyme, resulting in increased cholesterol secretion in bile (big risk for gallstones)

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10
Q

What is a major side effect of tPa?

A

Can cause reperfusion complex ventricular arrhythmias

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11
Q

What are the screening and confirmatory tests for treponema pallidum?

A

= syphillis

screening = PRP or VDRL

confirm = FTA-ABS

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12
Q

Sequelae of superficial Group A strep infections vs pharyngeal Group A strep infections

A

superficial: will present with yellow crusty blisters on face of a child –> can lead to poststrep glomerulonephritis (puffy face, dark/red pee)

pharyngeal = if untreated can lead to rheumatic fever (fatigue and heart murmurs)

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13
Q

What is the mechanism of action of an ACEi, what are the side effects?

A

blocks ACE, so no angiotensin II –> stops the efferent arteriole from constricting more than the affarent arteriol –> decrease glomerular pressure and GFR

Sdx: increase in creatinine, hyperkalemia, coughs

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14
Q

How is digoxin cleared?

A

Renally

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15
Q

What 3 enzymes require TLC For Noone cofactors, where are these enzymes used?

A

Pyruvate DH (convert pyruvate to actyl CoA)

aKG DH (a-KG –> succinyl CoA in TCA cycle)

a-ketoacid DH (used to breakdown I, L, V in MSUD)

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16
Q

B-blockers can be used to treat graves dz preparation for surgery

A

Apparently these will also help with the pts mood swings

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17
Q

What factors start the intrinsic and the extrinsic clotting pathway? What enzyme is used in the initial extrinsic path?

What test monitors these pathways?

A 
Intrinsic = XII (monitored by PTT)
Extrinsic = VII (enzyme that activates this = thromboplastin aka tissue factor) (monitored by PT-INR)
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18
Q

What would excess citrate do to the clotting cascade?

A

increased citrate binds free Ca. Ca is needed for many steps of the cascade, thus this would decrease clotting

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19
Q

What do protein C and S do?

Why do you have to give heparin with warfarin for the first few days?

A

Protein C and S block VIII and V (inhibit clotting from occurring.)

Warfarin will inhibit Factors 2,7,9,10 but bind Protein C and S FIRST (which can lead to transient hypercoagulable state when beginning treatment. Tx with heparin to give pt accurate decrease in clotting

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20
Q

What is the rate limiting step to the coag cascade?

A

Factor X activation

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21
Q

What do bradykinins do? What increases their synthesis? What blocks them?

What else do Kallikreins do?

A

Bradys are made from HMWK via Kallikrein (made by factor 12). Bradys can increase vasodilation, permeability, and pain. They are blocked by ACE

Kallikreins can also go on to increase plasmin synthesis from plasminogen. Plasmin can then go on to activate the compliment cascade!

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22
Q

Factor V Leiden

A

Mutation where FV is unresponsive to blockage by Protein C. This makes a hypercoagulable state

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23
Q

What is the antidote to heparin tox?

What is HIT and what is the antidote?

A

Protamine sulfate

HIT is the development of auto IgG Abs to the Heparin-PF4 complex. This complex activates platelets and causes TCP and thrombosis. Antidote = stop heparin and start on a Hirudin (lepirudin, bivalirudin.)

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24
Q

What are the advantages and disadvantages to LMWH

A

Disadvantages: act more on Xa and not on antithrombin

Advantages: can be given continiously, based on pt weight and not monitored constantly

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25
Q

What anti-coagulant is given for a.fib?

A

Warfarin

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26
Q

How do you overcome a warfarin OD?

A

vit.K or fresh frozen plasma

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27
Q

What is MOA of tPA/rPA/TNK-tPA?

How do you treat an OD?

A

Indirectly helps convert plasminogen to plasmin –> cleaves thrombin and fibrin (decreased clotting)

Leads to increased PT and PTT while no change in platelet count

Contrax: active bleeding, HTN, recent surgery

Tx for OD: Aminocaproic acid

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28
Q

What sites does fetal erythropoiesis occur at?

A 
YOUNG LIVER SYNTHESIZES BLOOD
Y: yolk sac (3-10 wk)
L: liver (6wk-birth)
S: spleen (15wk-30wk)
B: bone marrow (22wk to adult)
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29
Q

What blood type is the universal donor and recipient of RBCs?

Who is the universal donor and recipient of plasma?

A

Universal RBC donor = type O
Universal RBC recipient = AB

Universal Plasma donor = AB (no Abs present)
Universal Plasma recipient = Type O (already has all the Abs)

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30
Q

What type of RBCs will you see with Abetalipoprotienemia, Pb poisoning, DIC, metal heart valve, myelofibrosis, target cells, heinz bodies/bite cells, howell jolly bodies?

A

ABeta: Acanthocyte
PB: Basophilic stipling
DIC + Metal valve = Schistocyte
Myelofibrosis = teardrop cells
Target cells/Howel Jolly Bodies = Asplenia
(target cells also = thalassemia, and HbC disease)
Heinz/Bites = G6PD deficiency

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31
Q

What is the rate limiting step in heme synthesis? What cofactor is needed?

Where does this take place?

What inhibits this step?

A

ALA-synthase + B6

Occurs in the mitochondria

Glucose and heme will inhibit this step

32
Q

Acute intermittent porphyria

A

Defeciency in Porphobilinogen Deaminase –> increased levels of porphobilinogen, d-ALA. Uroporphyrin in the urine.

Presents like acute abdomin/neuropathy: stomach pain, polyneuropathy, port colored wine urine, and is precipitated by drugs

Tx: glucose and heme (to kill heme synth above the def.)

33
Q

Porphyria Cutanea Tarda

A

Def in Uroporphyrinogen Decarboxylase –> increased uroporphyrin in urine (tea colored)

Presents with tea pee, blistering photosensitivity w/ hair growth, dark face, alcoholism, and HCV (maybe)

34
Q

Lead Poisoning

A

creates a defective ferrochelatase AND ALA-dH (converts the last step in heme synthesis from protoporphyrin to heme)

causes microcytic hemochromic anemia w/ ringed sideroblasts (iron laden mitochondria inside RBCs seen in BM), MR, Stomach pain, dark gums, wrist/foot drop

Kids get it from eating paint
Adults get it from working in a battery/ammo factory

Tx: adults - EDTA/Succimer

35
Q

What are the pathogenicity and examples of Relative Polycythemia, Appropriate Absolute Poly, Inappropriate Absolute Poly, and Poly Vera?

A

Down Syndrome has an increased risk of Polycythemia

Relative = decreased plasma volume w/ normal RBC mass and O2 sat

Approp = increased RBC mass and decreased O2 sat. Can be due to Chronic Hypoxia (high alt, lung dz, sleep apnea)

Inapprop = increased RBC mass, normal others. Can be due to excessive EPO: RCC, Wilms Tumor, hepatocellular CA, ectopic usage

Poly Vera = Increased RBC mass and plasma volume due to benign RBC neoplasm. Itching after shower

36
Q

What makes the positive charge on histones? What is the only histone not to be part of the nucleosome core, what is its job?

A

histones = + charge via lysine and arginine

H1 is not a part of the nucleosome core, it links histones together

37
Q

What is the condensed form of DNA?

What does methylation and Acetylation do to DNA?

A

Condensed = heterochromatin

Methylation - inactivates

Acetylation - activates

38
Q

What amino acids are needed for purine and pyrimidine synthesis?

A

purine = GAG - glycine, aspartate, and glutamine (Carbons come from glycine, CO2 and THF, while Nitrogens come from aspartate and glutamine)

pyrimadines = Glutamine and Aspartate (Carbons come from CO2 and THF, Nitrogens come from asp and glut)

39
Q

What is orotic aciduria? How is it treated?

A

AR defect in UMP synthase –> cant make orotic acid into UMP

clx: megaloblastic anemia w/o hyperammonemia (This is different from OTC def (Urea cycle) where you would have hyperammonemia)

Tx: Oral uridine to bypass the defective enzyme. Cant be cured w/ B12

40
Q

What do the following enzymes do, and what drugs block them?

Ribonucleoside Reductase
Thymidylate Synthase
DHF reductase
PRPP Synthase
Ionisine Monophosphate
A

PYR path:

ribonucleoside reductase = UDP –> dUDP (blocked by hydroxyurea)
Thymidylate synthase = dUMP–>dTMP (blocked by 5-FU)
DHF reductase = DHF –> THF (blocked by MTX/TMP-bac)

PURINE path:
PRPP synthase = R5P –> PRPP (blocked by 6-MP)
Ionisine Monophosphate = IMP–>GMP (blocked by Mycophenolate)
DHF reductase works in this path too

41
Q

Lesch-Nyhan Syndrome

A

defective HGPRT (cant recycle GMP or IMP from guanine or hypoxanthine) resulting in excess uric acid production, w/ self mutilation, and gout

Tx: allopurinol for gout, but thats about it

42
Q

Adenosine Deaminase Def

A

cant make Inosine from adenosine –> decreases DNA synth and lymphocyte count –> SCID (triad)

43
Q

Silent vs Missense vs Nonsense vs Frameshift vs UV light mutations

A 
Silent - 3rd position, tRNA wobble
Missense - improperly folded, changed AA
Nonsense - stop codon
frameshift - truncated, nonfxl protein
UV light - thiamine-Thiamine Dimers formed on same strand of DNA
44
Q

Types of Prokaryotic DNA polymerase and their uses

A

Poly III = elongates leading strand (5 to 3 and proofreads w/ 3 to 5 exonuclease) and makes lagging strand

Poly I = degrades RNA primer 5 to 3

45
Q

Types of Eukaryotic DNA polymerase and their uses

A

alpha - lagging strand + RNA primer
beta/epsilon - repair strands
gamma - mitochondrial DNA
delta - leading strand

46
Q

Nucleaotide excision repair vs base excistion vs mismatch repair vs nonhomologous end joining PLUS dz for each

A

mismatch = specific endonuclease mediated; repairs bulky helix distortions. ex: Xeroderma Pigmentosa

Base Ex = Specific Glycosylases; used for single base repair. Used in spontaneous/toxic repair

Mismatch = recognized as the strand is formed. ex: HNPCC

Nonhomo= DS breaks. ex: Ataxia Telangiectasia

47
Q

Compare CPSI vs CPSII

A

CPSI - rate limiter in urea cycle, found in mitochondria and uses ammonia as its N source

CPSII - rate limiter in pyrimidine syth, found in cytosol, and uses glutamine as its N source

48
Q

What are the two causes of Trousseau’s sign? How are they different?

A

Hypocalcemia = carple muscle spasm with tightening of BP cuff

Pancreatic CA = migratory thrombitis (red hands/feet/extremities)

49
Q

What are the symptoms of Iron toxicity?

A

Gastric bleeding, erosion of stomach, emesis/hematochezia/ Can lead to hypovolemic shock.

Metabolic acidosis (a few hours later)

Scarring of GI tract (2-8wks later)

50
Q

What does a zinc def look like?

A

Poor wound healing, hypogonadism, decreased adult hair. Rash around mouth and anus

Also used in Carbonic Anhydrase, and Lactic DH

51
Q

Iron deficiency anemia

A

Cause: chronic blood loss, absorptive disorders, pregnancy
Clx: PICA, smooth red tongue (glossitis), esophageal webs (plummer vison)
Labs: Microcytic, hypochromic anemia

low Fe, low ferritin, hi TIBC & transferrin, low transferrin sat

52
Q

a-Thalassemia

A

Cause: a-globin gene mutation –> decreased lvls. cis deletion, in asians, trans deletion in africans. Different levels (as we have 4 a’s you can have worsening symptoms.)
Clx: 4 gene deltion = excess Hb(y) - Barts = hydrops fetalis (dead fetus)
3 gene deletion = HbH dz - excess B-globin (B4)

53
Q

B-Thalassemia Minor

A

Cause: B chain is underproduced, usually assymptomatic
Labs: elevated HbA2 (>3.5%) on electrophoresis w/ target cells
Clx: Micro, Homo anemia
More common in mediterranean

54
Q

B-Thalassemia Major

A

Cause: B-chain is absent
Clx: Micro, Homo anemia
severe anemia needing transfusions. (can lead to hemochromatosis.) Can see crew cut or chipmunk facies w/ target cells
Labs: Increased HbF (a2y2) to compensate for missing B

55
Q

Sideroblastic Anemia

A

Cause: X-linked defect in d-ALA synthase gene, alcohol, lead, isoniazid
Clx: Micro, Homo anemia
Labs: hi Fe, hi ferritin, normal TIBC w/ ringed sideroblasts (iron laded mitochondria found in BM)
Tx: B6 (cofactor for ALA-synthase

56
Q

Folate deficiency anemia

A

Cause: impaired DNA synth due to malnutrition, antifolates (MTX, TMP, Phen) or increased requirements (hemo anemia or pregnancy)
Clx: mecrocytic megaloblastic anemia
Labs: hypersegmented neutrophils w/ glossitis, low folate and hi homocysteine, NORMAL methylmalonic acid
Tx:

57
Q

B12 deficiency anemia

A

Cause: vegetarian, malabsorption, diphyllobothrium latum (fish tapeworm), PPIs
Clx: macrocytic, megaloblastic anemia w/ peripheral neuropathy
Labs: hyperseg. PMNs w/ glossitis, low B12, hi homocysteine, and high methylmalonic acid

58
Q

Nonmegaloblastic Anemias

A

Causes: liver dz, alcohol, 5-FU, AZT, hydroxyurea
Clx: a macrocytic anemia w/o hypersegmented neutrophils

59
Q

Intravascular hemolysis vs Extravascular hemolysis

A

Both cause normocytic, normochromic anemia

Intravasc: low haptoglobin, hi LDH, w/ hemoglobin in urine

Extravasc: macs in spleen clear RBCs, hi LDH w/ hi UCB causing jaundice

60
Q

Anemia of Chronic Disease

A

Cause: chronic inflammation –> increased hepcidin will bind ferroportin on intestinal mucosal cells/macs to block iron transport –> macs wont release iron
Clx: starts as a normocytic anemia, but can turn to microcytic, hypochromic after a while
Labs: low iron, hi ferriton, low transferrin and TIBC, high transferrin saturation

61
Q

Aplastic Anemia

A

Cause: failure/destruction of myeloid stem cells due to radiation, benzenes, viruses (parvo, EBV, HIV, HCV), Fanconi’s anemia (DNA repair defect)
Clx: fatigue, purpura, mucosal bleeding, infection
Labs: NO SPLENOMEGALY and pancytopenia w/ normal looking cells but a hypocellular bone marrow (LOW RET COUNT) w/ fatty infiltration
Tx: remove agent, give G-CSF or GM-CSF once immunosuppressed (grow some new BM)

62
Q

What is a direct and indirect coombs test?

A

coombs test = RBC agglutination w/ addition of antihuman Ab b/c RBCs are coated with IgG or complement proteins

Direct: You add Anti-human Abs to washed RBCs and they bind, thus the RBCs had IgGs on their surface already. (+) in hemolytic dz of newborn, drug-induced autoimmune hem anemia, hemolytic transfusion rxns

Indirect: You add pts serum to normal RBCs and see a presence of Abs in the serum. Use when testing to use blood prior to infusion, or screening moms Abs to fetus blood

63
Q

Hereditary Spherocytosis

A

Intrinsic, extravascular hemolytic normocytic anemia

Defect in spectrin = hi MCHC and RDW (some low MCV to mask microcytia) –> spleen kills RBCs

Pt will have splenomegaly, and can go into aplastic crisis if infected by Parvo B19

Labs: (+) fragility test lysing in NaCl solution
Tx: Splenectomy (will see howel jolly bodies after this

64
Q

G6PD deficiency

A

Intrinsic, Extravascular>Intravascular hemolytic normocytic anemia

X-linked def in G6PDH = RBC is without NADPH and thus susceptable to oxidative stress.

Pt will have back pain and hemoglobinuria a few days after stressor

Labs: Heinz bodies and Bite cells due to macs

65
Q

Pyruvate Kinase Def

A

Intrinsic, extravascular hemolytic normocytic anemia

low pyruvate kinase = no ATP = RBCs die in newborns

66
Q

HbC Defect

A

Intrinsic, extravascular hemolytic normocytic anemia

Glutamic acid –> Lysine mutation leads to a milder form of sickle cell like dz.

Labs: Hexogonal crystals in cells

67
Q

Sickle Cell Disease

A

Intrinsic, extravascular hemolytic normocytic anemia

Glutamic acid –> Valine mutation leads to sickling at low O2/dehydration. Newborns are not affected for a while due to high levels of HbF

Clx: crew cut, aplastic crisis risk w/ parvovirus, dactylitis (OFTEN FIRST SIGN IN KIDS), wedge shaped infarcts on spleen with eventual autosplenectomy

68
Q

Autoimmune hemolytic anemia

A

extrinsic, hemolytic normocytic anemia, Coombs +

Warm agglutinin = IgG mediated and caused by SLE, CLL, or a-methyldopa at HIGH temps

Cold agglutinin = IgM mediated and caused by CLL, Mycoplasma pneumonia, or EBV at LOW temps

69
Q

Microangiopathic Anemia

A

Extrinsic hemolytic normocytic anemia

RBCs damaged when passing through obstructed/narrowed vessel lumin. Ex: DIC, TTP-HUS, SLE, malignant HTN

Labs will show shistocytes (helmet cells)

70
Q

Macroangiopathic Anemia

A

Extrinsic hemolytic normocytic anemia

RBCs damaged when passing through big stuff: prosthetic heart valves, aortic stenosis

Labs show shistocytes

71
Q

Paroxysmal Nocternal Hemoglobinuria

A

Intrinsic, intravascular hemolytic normocytic anemia

Increased compliment mediated (Type III) RBC lysis due to mutation in hematopoietic stem cell disorder –> decreased GPI anchor or decay-accelerating factor that normally protects the RBCs.

Clx Triad: Hemolytic anemia, pancytopenia, venous thrombosis (big risk!) w/ red pee at morning

Labs: CD55/59 (-) RBCs on flow cyto. w/ a (+) Hams test (lysis at low pH)

Tx: Eculizumab

72
Q

What cells secrete elastase in the lung?

What can happen if too much is secreted? what stops this?

A

Alveolar macrophages or infiltrating neutrophils

Panacinar emphysema. a1-antitrypsin typically stops this from happening

73
Q

What is the anatomical cause of left ventricular outflow tract obstruction in a HCM pt?

A

Intraventricular septal hypertrophy and abnormal mitral valve motion

74
Q

What anti-clotting agent is used to prevent a DVT during surgery?

A

Heparin

75
Q

What cells take over as pacemakers when the heart goes into 3rd degree block (atria and ventricles are on their own separate rhythm)

A

AV node takes over (as long as QRS is still tight)

76
Q

What are the FEV1/FVC, TLC, and Diffusing Capacity in Emphysema?

A 
FEV1/FVC = decreased
TLC = increased
DC = decreased due to destruction of alveoli and adjoining capillary beds

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