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USMLE/ Step ONE > Mixed (9/20 --> 9/26) > Flashcards

Mixed (9/20 --> 9/26) Flashcards

1
Q

What is oxygen affinity of Hgb vs Myoglobin vs inidividual monomer of heme?

A

Myoglobin has one heme group, P50 of it is 1mmHg (very high O2 affinity).

Hgb has 4 heme groups (tetramer), P50 9s 26mmHg. However, as one O2 binds to a heme, affinity of other hemes for O2 increase!

One monomer of Hgb (i.e. tetramer breaks up into individual units) will act like a Myoglobin

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2
Q

MOA of Anti-Histamines

A

Reverse blockade =

Increase # of inactive H1 receptors

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3
Q

S/E of Anti-Histamines

A

Dry mouth
Blurry vision
Pee & Poop less

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4
Q

MC bugs causing bacteremia in hospital? Why devices responsible?

A

Staph aureus
Coag neg Staph
Enterococci
Candida

Intravascular devices; catheters

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5
Q

Compare Neurofibromatosis type 1 & 2: which chromosome & clinical Sx

A

NF-1 (von Reck. disease): Chr. 17
Sx: Cafe-au-lait spots, Lisch nodules (hamartoma on iris), many neurofibromas

NF-2 (central neurofibroma): CH 22
Sx: Bilateral acoustic neuromas

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6
Q

Which viruses are known to infect the dorsal root ganglia?

A

HSV-1, HSV-2

VZV

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7
Q

Which virus that infects DRGs have painful genital rashes? When does this happen in infection cycle?

A

HSV-2 (dsDNA virus)

rashes occur when latent virus reactivated

(reminder: DRG viruses: HSV1, HSV2, VZV)

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8
Q

In hemophilia A or B, addition of what helps in clotting?

A

Factor 8 (hemophilia A), Factor 9 (hemophilia B)

Thrombin

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9
Q

What pathway is tested by PT?

A

Extrinsic pathway

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10
Q

What is tested by PTT?

A

intrinsic pathway

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11
Q

Draw out the clotting cascade!

A

FA loser

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12
Q

Addition of what substance prevents thrombosis,and treats MI & PE?

A

Urokinase- Tx in MI and PE

converst plasminogen to plasmin, & degrades fibringogen & fibrin

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13
Q

How to test for Erectile dysfunction cause; Psychogenic (stress, anxiety, depression) or organic cause (Vascular, neurolog, trauma)

A

presence of morning erections rule out vascular, neurological, or genitourinary trauma

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14
Q

Which drugs cause impotence?

A

SSRI
Beta blockers
Methyldopa
Clonidine

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15
Q

Virulence factors; toxins of Bacillus anthracis and their MOAs, effects

A

2 virulence factors

1) antiphagocytic acid capsule
2) Trimeric anthrax toxin:
- Protective Ag (must be present for other 2)
- Edema factor: mimics adenyl cyclase-> ↑cAMP & (-) phagocytic cells

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16
Q

What is main Sx of anthrax and why?

A

Black edematous eschar borders, due to edema factor toxin

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17
Q

effects of pertussis toxin?

A

Edema & (-) of phagocytosis

(-)Gi-> ↑A.C. -> edema & phagocytosis dysfunction

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18
Q

Which Ag made by HBV noninfective? What is it’s significance?

Antibody to it indicates what?

A

HBsAg- noninfective envelope glycoprotein

(present in acute and/or chronic infection)

Anti-HBsAg = recovery & immunity

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19
Q

S/E of nonselective NSAIDs

A

Gastric ulcers
Renal ischemia
Bleeding; (-) PLTs
increase HTN (both COX 1&2 made in kidney)

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20
Q

Name COX-2 selective NSAID. Clinical use

A

Celecoxib

Clinical: RA, osteoarthritis. Patients w/ gastric ulcers and bleeding/ PLT problems (COX2 do not stop PLTs like COX1)

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21
Q

Where is COX1 & COX2?

A

Both made in renal tissue

Cox 2 also in vascular endothelium

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22
Q

S/E of COX2 (-)

A

Increase risk of thrombosis
(decreases PGI2 in endothelium, anti-clot)

Sulfa allergy

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23
Q

ACE (-) used cautiously in which group?

A

Patients w/ Renal artery stenosis
Heart failure
low fluid volume
Chronic kidney disease

Anyone dependent on efferent arteriole contriction (to keep GFR high enough)

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24
Q

how to tell if Cr variation due to ACE (-)?

A

If Cr goes up by 30% w/n 2-5 days of Rx therapy

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25
Q

stimulation of alpha-1 receptors effect?

A
  • ↑ systolic BP
  • Contraction of urethral sphincter
  • Mydriasis (contraction of pupillary dilator muscle)
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26
Q

Stimulation of Beta-1 receptors effect?

A

↑ HR, contractility, conductance

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27
Q

Stimulation of beta-2 receptor organ effect?

A
  • Vasodilation, decrease diastolic BP (skeletal muscle BVs)
  • Bronchodilation
  • Uterus relaxation
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28
Q

What drugs cause relaxation of uterus? How?

A

Beta 2 agonists relax uterus -> delay premature labor

Ritodrine & Terbutaline

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29
Q

When is liquifactive necrosis seen?

A

in CNS after strokes. Necoritc cells phagocytosed -> cystuc cavity made

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30
Q

Associations w/ coagulative necrosis?

A 
Organ ischemia (*myocardium, kidney*)
Exogenous injuries, like Brown recluse Spider bite
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31
Q

When do you see fat necrosis? Sapanification

A

Acute pancreatitis

Lipases digest parenchyma and make FAs.
Saponification occurs w/ FAs + Ca

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32
Q

What is Mallory-Weiss tear? Causes?

A

tear in gastric mucosa near stomach-esophagus junction.

Causes: Repetitive vomiting, strain during pooping & weightlifting, Upper GI endoscopy, abdominal injury

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33
Q

Effect of vomiting on pH, electrolytes?

A

Metabolic alkalosis

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34
Q

What condition has esophageal tear that causes air and/or fluid leak then into the mediastinum?

Sx?

A

Boerhaave syndrome

Septic shock, CHEST & upper abdominal pain, vomiting & retching

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35
Q

Preferred Tx od DKA? How long does this drug last?

A

regular Insulin. First as bolus, then IV

Works after 30min, lasts 5-8hrs

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36
Q 
List following insulin drugs for each:
Rapid-acting (3)
Short-acting(1)
Intermediate (1)
long acting (2)
A

Rapid (15min to work): Lispro, Aspart, Glulisine
Shor (30min)t: regular insulin
Intermediate: NPH (works in 2 hrs)
Long-acting: Detemir, Glargine (both last 24hrs)

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37
Q

MOA of ethosuximide?

A

block T-type Ca channels in thalamic neurons –> hyperpolarization

Used in Tx of absence seizures

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38
Q

Which drug decreases Na channel current , increasing neuronal refractory period?

A

Phenytoin
Carbazepine
Valproic Acid

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39
Q

What is Miliary TB?

A

Blood-borne dissemination of of Mycobacterium Tuberculosis to many organs from its quiescent start location

Presentation:
Tons of 1-3 mm, “Seedlike” White-Gray Lesions Caseous Lesions

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40
Q

How does congenital hypothyroidism present?

A

In infant soon after birth:

  • Muscle Hypotonia
  • Poor feeding
  • Jaundice
  • big tongue
  • Umbilical hernia
  • Myxedema
  • pale, dry, cool skin
  • myxedema
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41
Q

phases of HBV infection & immune response

A

Proliferative phase: liver cell expresses MHC I, HBsAg, &HBcAg. All used by CD8+ Tcells to respond by destroying infected liver cells

Integrative: cells that escaped prior immune response, virus incorporated into genome.

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42
Q

What causes secondary lactase deficiency?

A

Viral gastroenteritis

Lactase accumulate normally in microvilli of brush border. Virus damage this epithelium.

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43
Q

What is alternate name of lactose?

what is Lactose broken down into?

A

Lactose = Galactosyl beta-1,4 glucose

Galactose & Glucose (bound by 1,4 glycosidic linkage)

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44
Q

How to diagnose Celiac disease?

A

Small intestine biopsy

Shows flattening of mucosa w/ loss of villi & inflammation of lamina propria

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45
Q

Sx of Celiac disease?

A

Steatorrhea
Weight loss
Diarrhea
Deficiency of Vit, minerals

Cant handle gluten

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46
Q

Celiac sprue, explain? Site of impact

A

AutoAbs (IgA) to gluten (gliadin).

Affects distal duodenum or prox jejunm

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47
Q

What promotes new vessel growth in tumors, other than VEGF?

A

FGF

IL-1 & INF-gamma, indirectly do so by increasing VEGF

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48
Q

What is Oesophageal rupture ?

A

Oesophageal rupture (also known as Boerhaave’s syndrome) is rupture of the oesophageal wall. 56% of oesophageal perforations are iatrogenic, usually due to medical instrumentation such as an endoscopy or paraoesophageal surgery.[1] In contrast, the term Boerhaave’s syndrome is reserved for the 10% of oesophageal perforations which occur due to vomiting

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49
Q

What is timeframe for presentation and recovery of Maternity (Postparum) Blues?

A

Can start 2-3 days after delivery

Resolves w/n 10-14days

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50
Q

What are Sx of Postpartum Blues?

Tx?

A
  • Depressed affect
  • Tearfullness
  • Fatigue
  • Irritable

Tx: Supportive & Follow-up assess for possible Postpartum depression

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51
Q

How long does Postpartum Depression last? When does it start? What does it present w/?

A

Starts w/n 4 wks of delivery, can last 2wks to full year!

Sx: Anxiety, Poor concentration, Depressed affect. Sx are worse at night

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52
Q

How do you treat Postpartum depression?

A

Antidepressents

Psychotherapy

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53
Q

What is timeframe for postpartum psychosis? (when does it start, how long it lasts?)

A

Varies

4-6wks post-partum

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54
Q

What are Sx of Postpartum Psychosis?

Tx?

A

Delusions
Homicidal/suicidal attempts
Confusion
Hallucinations

Tx: Antidepressents, Antipsychotics, possible inpatient hospitalization

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55
Q

What are the stages of alcoholic liver disease? Which stages are reversible or irriversable?

A 
Hepatic Steatosis (reversible)
Alcoholic hepatitis (reversible)
Alcoholic cirrhosis (IRREVersible)
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56
Q

Describe Hepatic steatosis

A

Macrovesicular fatty changes

short-term change w/ moderate EtOH intake

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57
Q

What is alcoholic hepatitits?

A

Swollen necrotic liver cells w/ neutrophil infiltration

-mallory bodies present (intracytoplasmic Eosinophilic inclusions)

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58
Q

How to differentiate liver cell injury from liver cirrhosis?

A

Hepatocyte injury shows AST > ALT (1.5x or more), but doesn’t inmply anything about liver Fx

When liver disease severe where Fx affected, like alcoholic cirrhosis, patient has hypoalbumenemia & less coagulation factors (PT time prolonged). AST levels may or may not fluctuate.

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59
Q

What is alcoholic cirrhosis?

A

final, irriversible stage of liver disease

  • liver is shrunken w/ “hobnail” apearance.
  • Sclerosis around central vein (zone III)
  • Jaundice, hypoalbuminemia, high PT
60
Q

Describe the leads of a beventricular pacemaker; where they go in heart and how

A

Pacemaker that has leads for RA, RV, & LV

Leads to RA & RV enter via subclavian vein->SVC

Lead to RV goes from RA-> coronary sinus (located in AV groove, posterior side of heart

61
Q

Draw out the lysosomal storage disease chart

A

6 diseases, rxn parts

62
Q

What are the findings of Fabry’s disease?

A
  • Peripheral neuropathy of hands & feet
  • Angiokeratomas
  • cardiovascular/renal disease
63
Q

What enzyme is low in Fabry’s and what builds up?

A

enzyme low: alpha-galactosidase A

Ceramide trihexoside

64
Q

Gaucher’s disease Sx?

A
  • enlarged liver and spleen

- aseptic necrosis of femur, bone crises, Gaucher cells (macrophages that look like crumpled tissue paper

65
Q

What is enzyme low in Gaucher’s, what builds up?

A

low Glucocerebrosidase

buildup of Glucocerebroside

66
Q

All the Lysosomal storage diseases are AR, except?

A

Hunter’s & Fabry’s

both are XR

67
Q

presentation of Niemann-Pick disease

A
  • Progressive neurodegeneration
  • enlarged liver & spleen
  • cherry red spot on macula
  • foam cell
68
Q

Enzyme deficiency in Niemann-Pick disease. What increases?

A

Sphingomyelinase low

Sphingomyelin goes up

69
Q

How does ulnar claw present and how can it occur?

A

Ulnar nerve injury @ hook of hamate

Distal nerve lesion, like when falling on outstretched hand.

Cannot extend 4th & 5th digits

70
Q

Describe Tay-Sachs disease

A
  • progressive neurodegeneration
  • developmental delay
  • cherry-red spot on macula
  • lysosomes w/ onion skin
  • NO hepatosplenomegaly (like in NM-Pick)
71
Q

What enzyme low in Tay-Sach, what increases?

A

Hexosamindase A low

buildup of GM2 ganglioside

72
Q

Sx of Krabbe’s disease

A
  • Peripheral neuropathy
  • developmental delay
  • optic atrophy
  • globoid cells
73
Q

What is low and high in Krabbes

A

low Galactocerebrosidase

high Galactocerebroside

74
Q

What is Metachromic leukodystrophy

A
  • a lysosomal storage disease
  • Central and peripheral demyelination
  • ataxia
  • dementia
75
Q

Low enzyme in Metachroamtic leukodystrophy

A

Arylsulfatase A

buildup of Cerebroside sulfate

76
Q

What are the Pucopolysaccharidoses diseases?

A

Hurler’s Syndrome

Hunter’s Syndrome

77
Q

What are Sx of Hunter’s syndrome?

A
  • Mild Hurler’s + agressive behavior

- no corneal clouding

78
Q

What enzyme low in Hunter’s? What increases?

A

low Iduronate sulfatase

high Heparan sulfate & dermatan sulfate

79
Q

Hurletrs syndrome Sx?

A
  • Developmental delay
  • Gargoylism
  • Corneal clouding
  • airway obstruction
  • hepatosplenomegaly
80
Q

Low enzyme and high substrate in Hurler’s

A

low alpha-L-iduronidase

high heperan sulfate. dermatan sulfate (both also up in Hunter’s, but a different enzyme)

81
Q

What diseases higher in Ashkenaz Jews?

A

Tay-Sachs

Niemann-Pick

Gaucher’s

82
Q

What is a simple seizure?

A
  • A type of partial (focal) seizure

- remain conscious during seizure

83
Q

What are omelet seizures?

A

Memory loss

Type of partial (focal) seizure

84
Q

What are partial (focal) seizures?

A
  • Affect one area of brain, MC: medial temporal lobe
  • Seizure aura occurs before

-Types: simple partial and complex partial

85
Q

What is “aura” relating to seizures?

A

Sx that can occur before a seizure:

  • visual changes (bright lights, zigzag lines, spots, blind spots, distortions)
  • hallucinations (sound or smell)
  • unilateral numbness, tingling
  • feeling separated from body
86
Q

What is the first line Tx of partial seizures?

A

Carbamazepine

Also first line for tonic-clonic, like phenytoin & valproic acid
First line for trigeminal neuralgia too

87
Q

S/E of Carbamazepine

A
  • bone marrow suppression (all cell lines low)
  • liver toxicity, so watch LFT
  • induce SIADH
  • Steven Johnson syndrome
88
Q

What is Steven Johnson syndrome?

A

Prodrome (early Sx of a disease) of maialse and fever, followed by rapid onset of erythematous purpuric macules on mouth, eyes, and genitals.

Can progress to necrosis of epidermis and sloughed off.

89
Q

In relation to inguinal ligament, where do inguinal and femoral hernias occur?

A

Above ligament: inguinal hernia

Below ligament: femoral hernia

90
Q

Where do direct inguinal hernias protrude from? Give borers as well

A

Hesselbech triangle

Lower border: inguinal ligament
Medial: rectus abdominis muscle
Lateral: inferior epi gastric BVs

91
Q

Which type of hernia can protrude into scrotum?

A

Indirect inguinal hernia

92
Q

Where do indirect hernia protrude out of?

Where is this hernia in relation to inferior epigastric vessels?

A

Out of deep inguinal ring

Indirect hernia are lateral of inferior epigastric vessels, so, outside of Hesselbech triangle

93
Q

What are renal angiomyolipomas?

What other condition occurs with it 90% of time?

A

Benign tumor made of BVs, smooth muscle, and fat.

Associated with brain Tuberous Sclerosis

94
Q

What is Tuberous Scerlosis? How does it present (Sx)?

A

Cortical tubers and supependymal ham aromas in brain, that can result in seizures and mental retardation

Sx: cardiac rhabdomyomas, facial angiofibromas, leaf shaped patches on skin (ash leaf patches)

95
Q

How is deoxy-Hgb stabilized in tissues?

A

Tissue protons causes Hgb amino groups to be protonated->
Ion salt bridges made, stabilizing Hgb->
Decreases O2 affinity

96
Q

Explain proton levels in tissue elevated pO2 affect on proton in Hgb

A

Elevated proton in tissue due to CO2, which is converted to bicarbonate ions and & H+ ions by CA

Increased pO2 at alveoli increased O2 binding to Hgb, releasing protons.

97
Q

What factors decrease O2 affinity to Hgb?

A

Following cause right shift, decrease affinity of O2

“CADET, face right!”

Increase CO2, Acid, 2,3-DPG, Exercise, Temperature

98
Q

What is PKU and how does it present?

A

Low levels of phenylalanine hydroxylase prevent conversion of phenylalanine to tyrosine. Increased phenylalalanine (pa) causes:

  • mousy musty body odor
  • mental retardation
  • fair skin (pa [-] tyrosinase->melanin), eczema
  • seizures
99
Q

What is facilitation?

A

Technique to encourage patient to talk more about experience

I.e. “And then what happened?”

100
Q

What is empathy?

A

Expression of understanding of patients experience or difficulties. Trying to put yourself in patients shoes.

I.e. “I can imagine how the abuse has changed your views on life”

101
Q

What is the “reflection” technique when you interview?

A

You repeat what patient tells you, like, when summarizing:

“So, you’re telling me that you were raped as a child.”

102
Q

What is “support” technique during interview?

A

You show concern and interest in patient, but you don’t emphasize (try to relate)

I.e. “yes, he really hurt you. A lot of abused children have same reaction.”

103
Q

What can you ask elderly patient when you suspect abuse? (Patient alone at this point with you)

A

1) do you feel safe at home?
2) who prepares your meals?
3) who handles your checkbook?

104
Q

When infected with TB, what does macrophages release?

A

IL-12, which stimulates T cells to make IFN-gamma.

105
Q

What is role of IFN-gamma and TB infection?

A

After a macrophage infected with TB, it releases IL-12->
Tcell in response release IFN-gamma->
IFN-gamma activates Janus kinase 1&2->
Nuclear signaling results via STAT1 & transcription of IFN-gama regulated genes, which enhance intra cellular killing

106
Q

Cryptococcal neoformans infects CNS in what group?

A

HIV+ patients

Immunocompromised

107
Q

What is infection path of Cryptococcus neoformans?

A

Present in soil and pigeon droppings, yeast inhaled via respiratory route. Can spread to CNS.

108
Q

What test used to diagnose Cryptococcus neoformans?

A

India ink: Round or budding yeast with peripheral clearing (represents capsule)

Latex agglutination
Sabouraud culture
Methanamine stain

109
Q

What is periodic, non-peristaltic contractions of the esophagus called?

A

Diffuse Esophageal Spasm (DES)

Uncoordinated contractions of esophagus

110
Q

How does DES present?

A

Angina pectoris (chest pain)
Dysphagia
“Corkscrew esophagus” on barium swallow (due to simultaneous contractions)

111
Q

Effects of beta blockers in hyperthyroidism?

A

Two effects:
1) decrease effect of of catecholamines, reducing HR. During thyroid storm, there is increased sensitivity to catecholamines due to up regulation of beta receptors.

2) decrease conversion of T3 -> T4

112
Q

What explains quick recovery from barbiturate-like IV anesthetics?

A

Thiopental and other lipid soluble barbiturates in the brain rapidly redistribute into fats and muscles (5-10min) after administration. Plasma levels of drug, thus, drop rapidly.

Rapid plasma decay due to redistribution, NOT metabolism

113
Q

What are the types of macular degeneration?

A

Degeneration of macula (center of retina)

1) Dry type (non exudative) &
2) wet type (exudative)

114
Q

What are Sx of macular degeneration?

A

Distortion (metamorphopsia) & loss of central vision (CENTRAL SCOTOMAS)

115
Q

What is dry macular degeneration?

A

Deposition of yellowish fat beneath retina pigment epithelium (drusen) with gradual vision loss

116
Q

How to prevent progression of dry macular degeneration?

A

Multivitamin and antioxidant supplements

117
Q

What is wet (exudative) macular degenreration and how to treat?

A

Vision loss due to bleeding as a result of neovascularization.

Tx: laser or anti-VEGF injections

118
Q

When is drug effect additive?

A

Note the individual effect of two different drugs separately. If both given together, and their effect is exact sum of their individual effects, then both drugs have an additive effect!

Both drugs must have had some type of effect prior on their own for target.

119
Q

When does drug have synergic effect?

A

Note the individual effect of two different drugs separately. If both given together, and their effect is greater then the sum of their individual effects, then drugs work in synergy!

Both drugs must have had some type of effect prior on their own for target.

120
Q

When does a drug have a permissive effect?

A

One drug has no effect on a target, like cortisol on vascular reactivity.
2nd drug, NE has small effect on vascular reactivity.

When given together, cortisol leads to NE to have a strong vascular reactive response.

121
Q

What is acute inflammatory demyelinating polyradiculopathy?

Sx

A

Variant of Guillain-Barré syndrome. Tcells target, demyeliante, & destroy Schwann cells.

Sx:

  • ascending muscle weakness that starts in lower limbs
  • facial paralysis
  • increase CSF protein, normal cell count-> papiledema
122
Q

What is albuminocytologic dissociation?

A

Increased protein in CSF w/o increased cell count (like in infection)

Sign of Guillain-Barré syndrome

123
Q

What infection associated with Guillain-Barré syndrome.

A

CMV

Campylobacter jejuni

Autoimmune attack against myelin due to molecular mimicry.

124
Q

What condition has rapidly progressive leg weakness that ascends after a respiratory or GI infection?

A

Guillain-Barré syndrome

Acute autoimmune inflammatory demyelinating polyneuropathy

125
Q

What is critical in care of Guillain-Barré syndrome?

What is Tx?

A

** Respiratory support critical **

Tx: plasmapheresis, IV Abs

126
Q

What muscles and actions affected with damage to midshaft of humerus?

A

“BEST extensors”

Brachioradialis
Extensors of hand at wrist, and fingers.
Supinatior
Triceps

Wrist drop!!!!!!!

127
Q

Difference between incidence and prevalence.

A

Incidence number of new cases in a given period of time, prevalence measure of total number of cases at a point in time,

Prevalence = incidence * time

128
Q

MC cause of endocarditis with IV drug abuse?

A

S. aureus

129
Q

Why are pulmonary infarction hemorrhagic?

A

Dual blood supply of lungs

Bronchial and pulmonary arteries

130
Q

Most common presentation of IV drug abusers?

A

Endocarditis on right side of heart

Pulmonary infarction (<-develop septic emboli in lungs

131
Q

What animal can transmit Leprosy?

A

Armadillos

132
Q

What tissue does leprosy like to invade?

A

It likes cooler temperature, so superficial nerves and skin.

“Glove and stocking” loss of sensation

133
Q

Alternate name for Leprosy?

A

Hansen’s disease

134
Q

What is the the most severe form of leprosy? How does it present?

A

Lepromatous form.

  • Diffuse skin thinking
  • Hypopigmentation of plaques w/ hair loss
  • Blindness
  • Destruction of testicles
  • Leonine facies = loss of eyebrow, nasal collapse, lumpy earlobe
  • Sensory loss
135
Q

What is the mild form of leprosy and how does it present?

A

Tubercoid

Few hypoesthetic hairless skin plaques w/ minor sensory loss

136
Q

Describe immune response in both forms of leprosy

A

Lepromatous: low cell mediated immunity w/ humoral Th2 response.

Tuberculoid: high cell mediated immunity with large Th1-type immune response.

137
Q

During fasting, what processes maintain blood glucose levels?

A

First, glycogenolysis (first 12-18 hours)

Then, gluconeogenesis

138
Q

Role or pyruvate in gluconeogensis?

A

Pyruvate (derived from lactase, glycerol, glucogenic aa) a source for glucose.

Pyruvate becomes glucose via TCA cycle. Most important all allosteric activator is Acetyl CoA!

139
Q

Most important all allosteric activator for gluconeogenesis (pyruvate the source)?

A

Acetyl CoA most important. Acts (+) on PC enzyme.

In mito:
Pyruvate-(PC)->Oxaloacetate-(MD)->

Malate, leaves mito into cyto, becomes Oxaloacetate
-(PEPCK)-> Phosphoenolpyruvate-> glucose

140
Q

What CN sends afferent signal by carotid sinus stimulation (I.e. Carotid massage)?

A

CN 9 - glossopharyngeal

141
Q

What nerve is stimulated with stretching of aortic baroreceptors?

A

Vagus nerve (CN 10)

142
Q

Patient taking a drug for hyperlipidemia that causing skin flushing. What is the drug and what can be done to minimize this?

A

Patient taking Nicotinic Acid aka Niacin.

Skin flushing due to PGs, which can be kept under control with aspirin (given as pre treatment before niacin)

143
Q

How does Capsaicin reduce pain?

A

Reduces substance P, in PNS

144
Q

Patient with viral esophagitis and pneumocystis pneumonia, what do you think it is?

A

HIV+

145
Q

Diabetic mono neuropathy affects what CN? Explain path

A

Affects CN 3 causing nerve ISCHEMIA. specifically, the somatic function affected.

Patient has Ptosis, eyes down and out.
Normal accommodation and light reflex (parasympathetic fibers unaffected)

USMLE/ Step ONE (20 decks)

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