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Review / Wrong Answers > 6/19 UWorld > Flashcards

6/19 UWorld Flashcards

1
Q

What are the IV anesthetic choices

A
  • Benzos (conscious sedation for minor procedures)
  • Barbiturares (used for induction of anesthesia an short procedures)
  • Propofol
  • Etomidate
  • Ketamine
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2
Q

MOA and adverse effects of propofol

A

MOA: potentiates GABA-A

Adverse: CV effect (decreased in systolic BP)

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3
Q

MOA and adverse effects of Etomidate

A

MOA: potentiates GABA-A

Adverse effects: preserves CV stability

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4
Q

MOA and adverse effects of Ketamine

A

MOA: NMDA inhibitor

Adverse effects: CV stimulant, disorientation, hallucinations, unpleasant dreams,

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5
Q

What are the inhaled anesthetics

A

Nitrous oxide (non-volatile)

Halothane, Isoflurane, Enflurane (volatile)

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6
Q

Describe the difference in solubulity in blood, onset of action, and duration of action in volatile vs. non-volatile anesthetics

A
  • Non-volatile (N2O)
    • Less soluble in blood
    • Faster onset of action
    • Shorter duration
  • Volatile (e.g. Halothane)
    • More soluble in blood
    • Slower onset of action
    • Longer duration
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7
Q

What does blood:gas coefficient mean, and which has higher/lower - volatile or nonvolatile

A

Blood:gas coefficient = solubility in blood

Volatile anesthetics have higher blood:gas coefficient

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8
Q

What are adverse effects of all inhaled anesthetics

A

CV - mycardial depression, increased cerebral blood flow (due to decreased vascular resistance)

Respiratory depression (all inhaled anesthetics EXCEPT N2O)

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9
Q

Adverse effect specific to Halothane

A

Hepatic necrosis with 80% mortality

Halothane no longer used in US

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10
Q

Adverse effects specific to Enflurane

A

Nephrotoxicity

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11
Q

Drug causes of Malignant hyperthermia

A

VOLATILE inhaled anesthetics (not N2O) and Succinylcholine (depolarizing muscle relaxant)

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12
Q
A
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13
Q

Enzyme, substrate, and presentation of Fabry

A
  • XLR
  • Deficiency:
    • o Alpha-galactosidase
  • Accumulated substrate:
    • o Globotriaosylceramide
  • Presents with:
    • o Angiokeratoma
    • o Peripheral neuropathy
    • o Glomerulonephropathy
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14
Q
  • Enzyme, substrate, and presentation of Gaucher
A
  • AR
  • Deficiency:
    • o GLucocerebrosidase
  • Accumulated substrate:
    • o Glucocerebroside
  • Presents with:
    • o Hepatosplenomegaly
    • o Pancytopenia
    • o Bone pain/osteopenia
    • o Gaucher cell – lipid-laden macrophage with “crumpled tissue paper” appearance
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15
Q
  • Enzyme, substrate, and presentation of Tay Sachs
A
  • AR
  • Deficiency:
    • o Beta-hexoaminidase A (THINK: tay saX = heXaminidase)​
  • Accumulated substrate:
    • o GM2 ganglioside
  • Presents with:
    • o Macular cherry red spot
    • o Progressive neurodegeneration
    • o No hepatosplenomegaly
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16
Q
  • Enzyme, substrate, and presentation of Neimann Pick
A
  • AR
  • Deficiency:
    • o Sphingomyelinase​
  • Accumulated substrate
    • o Sphingomyelin
  • Presents with:
    • o Macular cherry red spot
    • o Progressive neurodegeneration
    • o Hepatosplenomegaly
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17
Q
  • Enzyme, substrate, and presentation of Krabbe disease
A
  • AR
  • Deficiency:
    • o Galactocerebrosidase
  • Accumulated substrate
    • o Galactocerebroside
    • o Psychosine
  • Presents with:
    • o Progressive neurodegeneration
    • o Peripheral neuropathy
    • o Optic atrophy
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18
Q
  • Enzyme, substrate, and presentation of Metachromatic leukodystrophy
A
  • AR
  • Deficiency:
    • o Arylsulfatase A
  • Accumulated substrate
    • o Cerebroside sulfate
  • Presents with:
    • o Progressive neurodegeneration
    • o Peripheral neuropathy
    • o Ataxia and dementia
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19
Q
  • Enzyme, substrate, and presentation of Hurler
A
  • AR
  • Deficiency:
    • o Alpha-L-iduronidase
  • Accumulated substrate:
    • o Heparin sulfate and dermatan sulfate
  • Presents with:
    • o Developmental delay
    • o Gargoylism
    • o Airway obstruction
    • o *Corneal clouding
    • o Hepatosplenomegaly
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20
Q
  • Enzyme, substrate, and presentation of Hunter
A
  • XLR
  • Deficiency:
    • o Iduronate sulfatase
  • Accumulated substrate:
    • o Heparin sulfate and dermatan sulfate
  • Presents with:
    • o Mild Hurler
    • o Aggressive behavior
    • o *No corneal clouding
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21
Q

Where are the location of B-cells, T-cells, and macrophages within the lymph node

A
  • B-cell
    • Located in follicle in the outer cortez
  • T-cell
    • Located in paracortex
  • Macrophages
    • Located in medullary sinuses
22
Q

What is located in the red pulp vs. white pulp of spleen

A

Red pulp = RBC

White pulp WBC

23
Q

Where is the location of B-cells, T-cells, and macrophages in the spleen

A

B-cells = germinal center of the follicle

T-cells = Periarteriolar lymphoid sheath (surrounding the central artery)

Macrophages = marginal zone (area between the red and white pulp

24
Q

What are the 4 possible fates of pyruvate?

A
  • Acetyl CoA via pyruvate dehydrogenase (TCA cycle)
  • Oxaloacetate via pyruvate carboxylase (gluconeogenesis)
  • Lactate
  • Alanine (urea cycle)
25
Vitamins needed for pyruvate dehydrogenase complex
B1, B2, B3, B5, Lipoic adi THINK: TLC For Nobody o T – Thiamin (B1) o L – Lipoic acid o C – CoA (B5) o FAD – Riboflavin (B2) o NAD – Niacin (B3)
26
What other enzyme needs the cofactors TLC For Nobody
alpha-keto glutarate dehydrogenase
27
What substance is inhibited by arsenic and what is the presentation of arsenic poisoning
Arsenic inhibits lipoid acid (T**_L_**C For Nobody) Clinical findings of arsenic poisoning: garlic breath, vomiting, rice-water stools, QT prolongation
28
Differentiate between pyruvate kinase deficiency and pyruvate dehydrogenase deficiency
* Pyruvate kinase deficiency * Cannot make pyruvate = no glycolysis = low ATP * Inability to maintain Na/K ATPase = RBC swelling and lysis * Pyruvate dehydrogenase deficiency * Buildup of pyruvate = lactic acidosis and neuro deficits * Treat with ketogenic diet (lysine and leucine)
29
Rate limiting enzyme of TCA cycle
isocitrate dehydrogenase
30
What step of the TCA cycle uses FAD+ to produce FADH2
Succinate --\> fumarate
31
What is the function of uncoupling agents
They uncouple the complexes of the electron transport chain from the final ATPase complex So instead of all the H+ that was pumped into the intermembranous space passing down gradient through the ATPase to generate ATP, the H+ just diffuse across the membrane on their own (not the the ATPase) and create wasted energy = heat production
32
Describe the fate of pyruvate that is converted to alanine
* Pyruvate + glutamate = alanine + a-ketoglutarate * Via pyruvate aminotransferase * Aminotransferases named based on NH3 donor * Alanine is the nitrogen transporter that will bring NH3 to the liver to participate in the urea cycle
33
What cofactor is neede for all aminotransferases
Pyridoxal phosphate (Vitamin B6)
34
What are the 4 important functions of NADPH
1. Fatty acid and steroid synthesis 2. Generation of O2 free radicals (O2 to O2- via NADPH oxidase) 3. Protection of RBC from O2 free radicals (via reduction of glutathionine) 4. CYP-450 enzymes
35
Describe the steps of oxygen free radical formation in phagolysosomes
O2 to O2- via NADPH oxidase O2- to H2O2 via superoxide dismutase H2O2 to HOCl via myeloperoxidase
36
What is the enzyme that takes over fructose metabolism in Essential fructosuria (fructokinase deficiency)
Hexokinase
37
Accumulated substrate and presentation of Galactokinase deficiency
§ Deficiency in galactokinase § Leads to accumulation of galacticol § Symptoms: · Infantile cataracts · Galactosemia and galactosuria
38
Deficieny enzyme and presentation of Classic galactosemia
§ Deficiency in galactose-1-phosphate uridyltransferase § Symptoms: · Infantile cataracts · Failure to thrive · Jaundice · Vomiting · Hepatomegaly · Renal dysfunction · Intellectual disability · E. Coli sepsis
39
What is the carb to calorie ration of protein, carbs, alcohol, and fatty acids
1 g carb/protein = 4 kcal 1 g alcohol = 7 kcal 1 g fatty acid = 9 kcal
40
What part of the body can ONLY use glucose for fuel
RBC Brain prefers glucose, but can use ketone bodies
41
What is the function of HMG CoA synthase in the mitochondria vs. cytosol
Mitochondria = ketogenesis Cytosol = choleserol synthesis
42
Why do you get fasting hypoglycemia after ethanol consumption
The liver will preferentially metabolize ethanol over glucose During ethanol metabolism, NAD+ is used up (via alcohol dehydrogenase) In order to regenerate NAD+, the liver converts pyruvate to lactate and oxaloacetate to malate Now there are no intermediates left to perform gluconeogenesis = fasting hypoglycemia
43
Function of chylomicrons
Delivers dietary TG to peripheral tissues Delivers cholesterol to liver in form of chylomicron remnants
44
Function of LDL
Delivers depatic cholesterol to peripheral tissues Take up by target cells via Clathrin-mediated endocytosis
45
Function of Apo E
Mediates remnant uptake On chylomicrons
46
Function of Apo A1
Activates LCAT (enzyme that esterifies cholesterol within HDL that was taken up from periphery\_
47
Function of Apo C2
LPL cofactor
48
Function of Apo B48
Mediates chylomicron secretion from enterocyte into lymphatics
49
Function of Apo B100
Bunds LDL receptor
50
Function of CETP (cholesterol ester transfer protein)
Transfers cholesterol esters from HDL to VLDL/LDL to be take back to the liver

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