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UW Flashcards

1
Q

How to Dx asthma?

A

Px & Hx
Spirometry ( FEV1 & PEF).
If spirometry is normal = methacholine challenge test.

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2
Q

How to interpret methacholine challenge test?

A

It’s a muscrinic cholinergic agonist.
Causes bronchoconstruction and increased airway secretions.
I.e FEV1 by >20%.

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3
Q

What’s scopolamine?

What is it used for?

A

Muscarinic receptor antagonist.

Used for motion sickness.

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4
Q

What’s phenoxybenzamine?

What does it treat?

A

It’s a non-selective a-adrenergic antagonist.

Used in pheochromocytoma.

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5
Q

What’s asthma?

A

Obstructive airway disease.

Hypersensitivity of conducting airways to stimuli.

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6
Q

Karyotype of turner’s?

A

45 XO

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7
Q

Clinical features of turners?
Menarche?
Labs?

A 
Short stature 
Thickened neck
Square chest
Widely spaced nipples. 
No breasts. 
Normal sexual hair distribution. 
No menarche.

High LH & FSH.

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8
Q

Can turner’s become pregnant?

A

They have ovarian failure, can’t.
Can use IVF with donor oocyte.

Need supplementation with estrogen & progesterone to maintain uterine lining.

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9
Q

What risk pregnancy has on turner’s women?

  • What’s your action?
A

Aortic dissection or rupture.

Must evaluate cardiac & renal function throughout pregnancy.

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10
Q

What are the signs of DKA?

A 
Mental status changes 
Dehydration 
Abdominal pain 
Tachypnea
Fruity odor of breath.

+
Metabolic acidosis & high AG.

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11
Q

What are the finding of DKA on ABG?

A

Metabolic acidosis
With high anion gap.

PH

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12
Q

Treatment of DKA?

How does it work?

A

Insulin & hydration with NS.

• Insulin:
Utilization of glucose > lipolysis > normalizes glucose & stop Keton bodies = increased HCO3.

Intercellular shift of K = K in blood.

• NS:
Normalizes Na in blood & decreases osmolality.

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13
Q

Describe ABG changes is hypoaldosternism (RTA IV)

A

Metabolic acidosis with normal AG.

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14
Q

Treatment of metabolic acidosis in hypoaldosternism?

How does it work on ions, acids & osmolality?

A

Exogenous mineralocorticosteroids.

  • Na/H2O retention.
  • H & K excretion > hypokalemia & ⬆️HCO3.
  • Increases serum osmolality.
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15
Q

How does loop diuretics affect ions, acids & osmolality?

A

• Decrease Na/H2O retention:
Low Na, low fluids > high serum osmolality.

  • Loss of K = Hypokalemia.
  • Retains HCO3.
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16
Q

What causes fruity smell of breath and urine in DKA?

A

Excretion of acetone

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17
Q

What 2 acids accumulate in DKA?

A

B-hydroxyburate

Acetoacetate

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18
Q

What’s minute ventilation?

How is it calculated?

A

It’s the volume of air that enters the respiratory pathways per minute.

Minute Volume = tidal volume x RR

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19
Q

What’s alveolar ventilation?

How is it calculated?

A

Volume of air reaching alveoli per minute i.e doesn’t include dead space.

Alveolar ventilation = (Tidal volume - dead space) x RR

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20
Q

What’s physiologic dead space?

How is it calculated?

A

Anatomical (conducting airways) and alveolar (well ventilated but poorly refused alveoli) dead space.

Physiological dead space = tidal volume x ([PaCO2 - PeCO2] / PaCO2)

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21
Q

During what stage of cardiac cycle does most of blood supply to myocardium occur?

What’s the major factor affecting myocardial blood flow?

Why?

A

80% of blood supply is during diastole

And depends mostly on duration of diastole.

Why?
Systole => the open aortic valve partially blocks coronary flow and coronary arteries are compressed by the contracting myocardium.

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22
Q

What happens to cardiac supply during exercise?

A

⬆️ HR and ⬇️ diastole
> more demand and less time to provide oxygen.

Adenosine (from ATP) vasodilates coronary vessels and increases blood flow.

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23
Q

What’s the type of inheritance in CF?

A

Autosomal recessive

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24
Q

Where’s the defect in CF?

A

Cystic fibrosis transmembrane conductance regulator (CFTR) gene on chromosome 7.

F508 mutation.

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25
Q

What’s the F508 mutation?

What does it cause?

A

Deletion of 3 nucleotides coding for phenylalanine at position 508 of the CFTR protein.

Causes CF.

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26
Q

What’s the CFTR transmembrane protein and what does it pump?

How is it related to mucosal surfaces?

A

An ATP-binding cassette transmembrane ion transporter.

Pumps Cl out of epithelial cells against its concentration using ATP hydrolysis for energy.

By pumping Cl it creates a membrane potential that draws Na and H2O which hydrates mucosal surfaces like bowels and airways.

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27
Q

What’s the role of CFTR protein in sweat formation?

A

It plays a role in forming a hypotonic sweat.

Sweat is initially isotonic with the plasma, during transport through the ducts Na is removed from the ductal lumen by CFTR.

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28
Q

What’s the effect of CFTR defect on sweat in CF patients?

A

CF patients have high Cl in sweat

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29
Q

What test is used to screen for CF?

A

Sweat Cl Test.

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30
Q

Where are voltage-gated channels commonly found?

A

In neurons.

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31
Q

What’s the function of LH in males?

A

Stimulates the release of testosterone from the lyeding cells.

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32
Q

Where is LH released from?

A

Gonadotroph cells in the anterior pituitary.

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33
Q

What’s the function of FSH in males?

A

Release of inhibin B from the Sertoli cells in seminefrous tubules.

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34
Q

What’s the karyotype of Turners Syndrome?

A

45, XO (loss of paternal Ch X)

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35
Q

Classic Characteristics of newborn with turner’s syndrome?

A
  • Cystic Hygroma = posterior neck mass of cystic spaces.
  • Lymphedema = Bilateral extremities swelling.
  • Coarctation of aorta = diminished femoral pulses.
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36
Q

What’s the pathology in congenital adrenal hyperplasia?

What’s the most common enzymatic defect?

A

Abnormal sexual differentiation due to defective hormone synthesis.
Most common enzymatic defect = 21-OH deficiency.

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37
Q

How do newborn with congenital adrenal hyperplasia present?

A

Girls have ambiguous genitalia and salt wasting (hypotension & low Na)

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38
Q

What’s the cause of pathology in androgen insensitivity syndrome?

A

Defective testosterone receptors.

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39
Q

What is the karyotype in androgen insensitivity syndrome?

A

46, XY

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40
Q

How do patients with androgen insensitivity syndrome present? (Phenotype)

A

Adolescent 46,XY how appears phenotypic ally female, has primary amenorrhea.
Presence of cryptorchid testes.

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41
Q

What’s the cause of primary amenorrhea in androgen insensitivity syndrome?

A

Absence of internal female reproductive tract.

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42
Q

What’s the cause of pathology in Trisomy 18 (Edward Syndrome)?

A

Meitotic nondisjunction.

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43
Q

Mention some of the symptoms of Trisomy 18?

A 
Cardiac defects. 
Clenched fists. 
Rocker bottom feet. 
Omphalocele. 
Low set ears.
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44
Q

What’s the cause of pathology in Cri-du-chat?

A

Deletion of the short arm of Ch 5 (p5-)

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45
Q

What is the cause of pathology in Trisomy 21?

A

Meiotic nondisjunction

Robertsonian translocation.

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46
Q

What’s the mode of inheritance in Fragile X?

A

X-linked.

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47
Q

What’s the molecular cause of pathology in Fragile X?

A

Increased number of trinucleotide repeats (CGG) in familial mental retardation gene (FMR-1)

48
Q

What are the symptoms of Fragile X syndrome?

A

• Body Habitus:

  • Macrosomia => increased head circumference.
  • Large jaw.
  • Large protruding ears.
  • Long thin face.
  • prominent forehead.
  • Large testis.

• Cognitive impairment:

  • mental retardation.
  • Language delay.
  • Behavioral abnormalities (aggressiveness).
  • Autistic features.
49
Q

What’s Genome Recombination?

A

Gene exchange between 2 chromosomes that occur via crossing over within homologous regions of 2 ds-DNA.

50
Q

What’s genome re-assortment?

A

Changes in genomic composition.

In viruses its when 2 segmented viruses exchange whole genome segment.

51
Q

What’s the embryonic origin of SVC?

A

Common Cardinal veins

52
Q

On an chest CT, how do you identify the SVC?

A
  • Right to the heart
  • Posteriolateral to ascending aorta.
  • Anterior to Rt pulmonary artery.
  • Below the carina.
53
Q

Where do veins in embryo drain into?

A

Sinus venosus => primitive atrium.

54
Q

What are the main categories of veins in embryo?

What do they give rise to after birth?

A

• Vitelline, umbilical & Cardinal veins.

• umbilical vein = degenerates.
Vitelline vein = veins of portal system.
Cardinal veins = veins of systemic circulation.

55
Q

What develops from the truncus arteriosus?

A

Ascending aorta & pulmonary trunk.

56
Q

What gives rise to descending aorta?

A

Fusion of embryonic Rt&Lt dorsal aortas

57
Q

How does truncus arteriosus form the ascending aorta & pulmonary trunk?

A
  1. Migration of neural crest cell migration = fusion & twist of truncal & bulbar ridges.
58
Q

What causes opening snap in MS?

A

Abrupt halting of leaflet motion during mitral valve opening due to fusion of leaflet tips.

59
Q

What’s the most common cause of MS?

A

Rheumatic carditis.

60
Q

What’s the murmur of MS?

A

Opening snap followed by diastolic rumble

At the apex of the heart.

61
Q

What’s paroxysmal supraventricualr tachycardia?

What patients get this commonly?

A

Abrupt episodic onset of rapid HR and termination.

Due to re-entrant impulse traveling through rapidly and slowly conducting segments of AV node.

Patients with no heart disease.

62
Q

Ex of Paroxysmal supraventricualr tachycardia?

A

1) Cardiac parasympathetic stimulation
> carotid sinus message & valsalva maneuver.
> parasympathetic => prolonged AV node refractory period => slow conductance through AV => Slow HR.

2) Adenosine

63
Q

Compression of hypertrophic / dilated left atrium presents as?

A

Dysphasia

64
Q

What are the 4 major divisions of the aorta & what’s their anatomical position?

A
  1. Ascending aorta = posterior & Rt to the main pulmonary artery
  2. Aortic arch = above the right pulmonary artery & left bronchus.
  3. Descending thoracic = left anterior surface of vertebral column & posterior to esophagus and left atrium.
  4. Descending abdominal = crosses diaphragm & branches into common iliac arteries.
65
Q

How is the position of thoracic aorta helpful in TEE?

A

It lies posterior to esophagus & left atrium

Allowing clear visualization during TEE, which helps in detecting dissections or aneurysms.

66
Q

Penetrating injury to left-sternal border in 4th ICS will pass through what layers?

A
  1. Skin & subcutis
  2. Pectoralis major
  3. External intercostal membrane
  4. Internal intercostal muscle.
  5. Internal thoracic artery & vein.
  6. Transverse a thoracis muscle.
  7. Parietal pleura.
  8. Pericardium.
  9. Rt ventricular myocardium.
67
Q

Penetrating injury to 2nd intercostal space result in injury to?

A

Pulmonary trunk

68
Q

Stab wound to 4th ICS midclavicualr line injures what structures?

A

Left lung & left ventricle.

69
Q

Most common cause of blunt aortic injury?

Mechanism of injury?

Most common site of rupture? Why?

Dx?

A

Motor vehicle collisions

Sudden deceleration.

Aortic isthmus, tethered by ligamentum arteriosum => fixed and immobile.

Widened mediastinum on CXR.

70
Q

Drugs that cause long QT interval?

Hint: ABCDE

A 
Antiarrythemics (Class IA + III)
Antibiotics (macrolides)
Anti-psychotics (haloperidol)
Anti-depressant (TCA)
Anti-emetics (ondansetron)
71
Q

What are the HMG-CoA reductase inhibitors?

What’s their mechanism of action?

Most common side effects?

A
  • lipid lowering agents (Statin group)
  • Inhibit the conversion of HMG-CoA to mevalonate (cholesterol precursor).
    Work mainly on LDL.
  • Hepatotoxicity (high LFT)
72
Q

What’s supine hypotension syndrome?

What’s the cause?

Who usually gets it?

A

Hypotension, sweating, nausea & dizziness when a pregnant woman lies supine.

Secondary to the uterus compressing IVC leading to reduced venous return and low CO & hypotension. Syncope if sever.

Pregnant ladies > 20 wks gestation.

73
Q

What equations are used to calculate the CO?

A
  1. CO = HR x SV
  2. Fick Principle.
    CO = O2 Consumption / arteriovenous O2 difference.
  3. Using Hb & body surface area.
    CO = (135 x BSA) / [(13 x Hb) x (SaO2 - SvO2)].
74
Q

What’s the Resp quotient?

What’s its normal value?

What’s it used for?

A

It’s the ratio of CO2 to O2 across alveolar membrane.

Normal value 0.8

Used to estimate metabolic rate.

75
Q

What allows pacemaker cells in the heart to exhibit automaticity?

A

The slow inward Na current (funny current) during phase 4.

76
Q

How is the IVC formed and where does it drain?

A

IVC is formed by the Union of the art & Lt common iliac veins at the level of L4-5.
Drains into the Rt atrium at level of T8.

77
Q

Thoracic vs cystic duct.
Function
Anatomical location.

A
  1. Thoracic duct:
    - Drains lymph from the entire left side of the body and all regions inferior to umbilicus.
  • enters the thorax through the aortic hiatus & empties into the left subclavian vein near its junction with internal jugular vein.
  1. Cystic Duct.
    - drains bike from the gallbladder into the common bile duct.
  • it lies just below the liver in the anterior Rt abdomen.
78
Q

What makes up the portal vein?

Where is it anatomically?

A
  • joining of superior mesenteric vein & splenic vein.

- near the head of pancreas.

79
Q

Where do renal arteries originate anatomically? (Vertebral level)

A

Level L1.

80
Q

How does the body respond to hypovolemic shock?

A

After losing 10% of circulating volume sympathetic nervous system is activated and leads to:

  1. Construction of arterioles:
    Increase TPR
    Maintain end-organ pressure & shunt the blood from extremities & skin to vital organs.
  2. Construction of veins:
    Increases VR and maintain preload.
  3. Stimulation of the heart:
    Increases contractility and HR.
81
Q

What’s the mainstay treatment in hypovolemic shock?

What’s the mechanism of action?

A
  • rapid infusion of blood products & NS
  • IVF increase intravascular volume & ventricular preload.
    Increased preload = extended end diastolic sarcomere length = high SV & CO.
82
Q

What’s the cause of high TPR in hypovolemic shock?

A

Sympathetic stimulation.

83
Q

What’s the effect of IVF on HR & TPR in patients with hypovolemic shock?

A

Decrease HR & TPR.

By reducing sympathetic activation.

84
Q

What effects ventricular compliance?

A

Increases by = dilated cardiomyopathy.

Decreased by = amyloid deposition & hypertrophic cardiomyopathy.

85
Q

Holo systolic murmur is characteristic of what heart disease?

How do you differentiate them?

A

Mitral & tricuspid regurgitation and VSD.

TR is associated with increased intensity during inspiration while MR & VSD are not.

TR is heard at left eternal border at 4th ICS.
MR is at 5th ICS midcalvicular line.
VSD at 3rd/4th ICS left sternal border.

86
Q

What causes increased intensity of TR murmur during inspiration?

A

During inspiration intra-thoracic pressure drops, allowing more blood to return to Rt heart > Rt ventricular SV increases > increased capacity of Rt pulmonary vessels > low VR to left ventricle.

87
Q

What’s the effect of the following on cardiovascular:

  • NO
  • Adenosine
  • Norepinephrine
  • Ach
  • Ang-II
  • Histamine
  • Serotonin
A
  • NO:
    From endothelium.
    Vasodilator of large coronary vessels.
  • Adenosine:
    From ATP metabolism.
    Vasodilator of small coronary vessels.
  • Norepinephrine:
    Neurotransmitter released from SNS to stimulate alpha-receptors.
    a1-receptors > construction of vessels.
    a2-receptors > inhibit sympathetic system centrally.
    B1-receptors > cardiac excitation.
  • Ach:
    Neurotransmitter from PNS. Acts on muscarinic receptors > inhibitory effect on heart.
  • Ang-II
    Powerful vasoconstrictor.
  • Histamine:
    From mast cells.
    Potent vasodilator
  • serotonin:
    From neuroendocrine cells, platelets, serotonergic neurons.
    Both vasodilation & constriction.
88
Q

How & where is NO made?

How does it act?

When is it released?

A

It’s made by endothelial cells.

It’s synthesized from arginine and oxygen by enzyme eNOS (endothelial nitric oxide synthase.

Vasodilates vessels via guanylate cyclase enzyme to increase the production of cGMP & cause ms relaxation.

Released in response to:

  1. Neurotransmitters (Ach & NE)
  2. PLT products (serotonin, adenosine & diphosphate).
  3. Thrombin
  4. Histamine
  5. Bradykinin
  6. Endothelin.
  7. Pulsatile stretch & flow shear stress.
89
Q

What’s the function of AV node?

A

Has a refractory period to regulate the number of atrial impulses that reach the ventricle and determines the ventricular rate.

90
Q

What’s the pathology in A-Fib?

Characteristic ECG?

A

Aberrant electrical impulses that arise within regions of high atrial excitability (pulmonary veins) > electrical remodeling & shortened refractory periods with increased conductivity.

Resulting in persistent ectopic foci & re-entrant impulses within the atria.

Characteristic ECG: absent P waves, irregular R-R intervals & narrow QRS complexes.

91
Q

What determines the duration of QRS complex ?

A

Bundle branch conductivity.

Thus when there’s a branch block QRS is widened.

92
Q

What vessels supply myocardium?

A

Rt & Lt coronary arteries which originate from the root of aorta behind the 2 cusps of aortic valve.

93
Q

Where do the coronary veins drain?

A

Coronary sinus in right atrium.

94
Q

What features distinguish coronary from systemic circulation?

A
  1. Cardiac muscles is mostly prefixed during diastole & consumes 5% of CO.
  2. Cardiac oxygen extraction reaches 75 - 80% of oxygen content at rest and 90% at demand.
  3. Flow regulated by local metabolites NO, adenosine, Beta adrenergic activity for vasodilation
    Alpha adrenergic for vasoconstriction.
95
Q

Which is more deoxygenated:
Pulmonary artery or coronary sinus?

Why?

A

Coronary sinus.

Blood from coronary sinus which is extremely deoxygenated is mixed with blood from IVC which is less deoxygenated and thus the blood in pulmonary artery contains a mixture of the 2 and is less deoxygenated from the coronary sinus blood.

96
Q

What’s the effect of AV shunt of pressure-volume loop?

A

1) AV shunts increase preload => increase rate and volume of VR.
2) AV shunts allow blood to bypass the arterioles => low TPR.

So elongated diastolic filling phase, high EDV and low after load.

97
Q

What’s the end result of AV shunt?

A

High output heart failure.

98
Q

What determines resting potential in cardiac muscle?

A

Membrane permeability for K

99
Q

What’s the benefit of highly negative resting potential in cardiac muscle?

A

Reduce risk of arrhythmias.

100
Q

What characterizes plateau phase in cardiac muscle AP?

A

Opening of L-type dihydropyridine-sensitive Ca channels

Closure of K channels.

101
Q

Relate each pharyngeal arch with its corresponding aortic arch, CN & derivatives.

A

• 1st pharyngeal arch:
1st Aortic arch => maxillary artery
Trigeminal nerve CN V

• 2nd Pharyngeal arch:
2nd aortic arch => Stapedial artery.
Facial nerve CN VII

• 3rd Pharyngeal Arch:
3rd aortic arch => common carotid artery & proximal internal carotid
Glossopharyngeal CN IX.

• 4th Pharyngeal Arch:
4th aortic arch => true aortic arch & subclavian arteries.
Superior laryngeal branch of vagus.

• 5th Pharyngeal Arch:
Obliterated

• 6th Pharyngeal Arch:
6th aortic arch => pulmonary arteries & ductus arteriosus.
Recurrent laryngeal branch of vagus.

102
Q 
Define the following terms:
• Permissive effect 
• Synergic effect 
• Additive effect 
• Tachyphylaxis
A

1) Permissive:
One hormone allows another to exert its maximal effect.
I.e cortisol up-regulates a1-adrenergic receptors and augment catecholamines & Ang-II vasoconstrictive effect.

2) Synergistic effect:
The combined effect of 2 drugs exceeds the sum of the individual drug.

3) Additive effect:
The combined effect of 2 drugs equal to the sum of their individual effects.

4) Tachyphylaxis:
Decreased drug responsiveness in a short period following one or more doses (rapid tolerance)

103
Q

What are the therapeutic uses of GnRH depending on frequency of administration?

A

Pulsatile GnRH agonists => stimulates LH & FSH => Rx infertility.

Constant GnRH or long lasting analogue => Suppress LH & FSH => Rx precious puberty, prostate ca, endometriosis & dysfunctional uterine bleeding.

104
Q

What’s the function of GnRH?

A

Secretion of LH & FSH => development of dominant follicle in ovaries.

105
Q

Mention the signaling pathway of insulin.

A

Insulin binds a-subunit of its the receptor => autophosphorylation of receptor => ctivation of tyrosine kinase => interaction with receptor substrate 1 & 2

106
Q

What’s the effect of TNF-alpha on insulin?

How?

What other substances exhibit similar effect?

A
  • causes insulin resistance.
  • By phosphorylation of insulin receptor substrate 1 serine residues => inhibiting tyrosine phosphorylation => insulin resistance.
  • substances the phosphorylate threonine residues = catecholamines, glucocorticoids, glucagon.
107
Q

What inactivates cAMP?

A

Hydrolysis of phosphodiestrase

108
Q

What’s hydroxyproline used for?

How is it formed?

A
  • used in synthesis of bone, skin & collagen.

- formed by hydroxylation of proline which requires vit c

109
Q

What’s peroxisome proliferator-activated receptor gamma (PPAT-gamma)?

What’s its effect on insulin?

What drugs activate it?

A

It’s a nuclear receptor that alters gene transcription.

Improves insulin sensitivity.

Oral anti-diabetics (thiazolidinediones TZD).

110
Q

What’s lecithin-sphingomyelin ratio used for?

A

Marker for fetal lung maturity.

> 1.9 indicative of mature lung.

111
Q

What factors fetal lung development and how?

A

By increasing surfactant.

Glucocorticoids (most imp)
Prolactin 
Insulin 
Estrogen 
Androgen 
Thyroid hormones
Catecholamines
112
Q

What’s the function of thyroid perixidase?

A

Catalyzing enzyme

  • Oxidation of iodide into iodine.
  • Coupling of TID & MID.
113
Q

Antibodies against thyroid peroxidase result in what disease?

A

Hashimoto’s

114
Q

What are the basic amino acids?

A

Lysine, arginine & histidine.

115
Q

What’s the function of aromatase enzyme?

A

Converts androgens (androstenedione) to estrogen & testosterone to estradiol at the peripheral tissues.

116
Q

Clinical manifestations of aromatase deficiency on mom & baby.

A
  • Mom => virilization e.g hirsutism.
  • Baby girl => normal internal female genitalia & ambiguous external genitalia (clitormegaly & pseudohermaphrodism)

At puberty => primary amenorrhea, osteoporosis & tall stature.

117
Q

What’s the effect of 5a-reductase deficiency?

A

Decreased dihydrotestosterone in male.

=> undeveloped external male genitalia

USMLE (3 decks)

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