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Physiology Flashcards

1
Q

U waves in EKG are seen in:

A

Hypokalemia

Bradycardia

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2
Q

First cardiac sound is due to:

A

Mitral and tricuspid valve closure

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3
Q

Second cardiac sound is due to:

A

Aortic and pulmonary valve closure

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4
Q

S3 (gallop) is due to and can be associated with:

A

Fast ventricular filling or filling an already full ventricle
In eccentric hypertrophy (dilation)
Congestive heart failure and mitral regurgitation

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5
Q

S4 is due to and can be associated with:

A

Atrial kick
Indicates an stiff ventricle
In concentric hypertrophy
Hypertension and aortic stenosis, hypertrophic cardiomyopathy

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6
Q

Component of the jugular venous pulse absent in tricuspid regurgitation:

A 
X descent (atrial relaXation)
Absent in tricuspid regurgitation
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7
Q

Holosystolic high-pitched blowing murmur indicates:

A

Mitral/tricuspid regurgitation

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8
Q

Crescendo-decrescendo systolic murmur indicates:

And other characteristics associated with this murmur:

A

Aortic stenosis

Associated also with pulsus parvus et tardus

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9
Q

Holosystolic harsh-sounding murmur indicates:

A

Ventricular septal defect

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10
Q

Late systolic crescendo murmur with midsystolic click indicates:

A

Mitral valve prolapse

That it’s the most frequent valvular lesion

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11
Q

High-pitched blowing early diastolic decrescendo murmur indicates:
And other characteristics associated with this murmur:

A

Aortic regurgitation

Associated also with bounding pulses and head bobbing

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12
Q

Delayed rumbling late diastolic murmur indicates:

And other characteristics associated with this murmur:

A

Mitral stenosis

It follows opening snap

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13
Q

Continuous machine-like murmur indicates:

A

Patent ductus arteriosus

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14
Q

Heart rate is determined by which component of the pacemaker action potential?

A

By the slope of phase 4 in the SA node

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15
Q

Which infection can result in a 3rd-degree heart block?

A

Lyme disease

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16
Q

Which heart block can Lyme disease lead to?

A

3rd-degree heart block

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17
Q

Intrapleural pressure at FRC:

A

Negative, small change ~-5cm H2O

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18
Q

Chromaffin cells in adrenal medulla are stimulated by and secrete:

A

Stimulated by Ach released by sympathetic preganglionic neurons

Segregate epinephrine and norepinephrine

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19
Q

Preload is approximated and decreased by:

A

End-diastolic vol.

vEnodilators

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20
Q

Afterload is approximated and decreased by:

A

Mean arterial pressure

vAsodilators

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21
Q

Ach is released on the synapses at:

A

Neuromuscular junction
Both sympathetic and parasympathetic ganglia
Postganglionic parasympathetic organ target

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22
Q

NE is released on the synapses at:

A

Postganglionic sympathetic organ target (the adrenal acts as the sympathetic ganglia)

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23
Q

G protein, hormones that bind to it and second messenger of beta receptors:

A 
Gs prot (where epi, glucagon, TSH and PTH bind)
Activates adenyl cyclase to increase cAMP
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24
Q

G protein and second messenger of alpha 1 receptors:

A

Gq prot

Activates phospholipase C that generates IP3 and DAG

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25
Q

G protein and second messenger of alpha 2 receptors:

A

Gi prot

Inhibits adenyl cyclase to decrease cAMP

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26
Q

Characteristics of the holosystolic murmur in mitral regurgitation:

A

Best heard at apex and left lateral decubitus
Radiates to the axila
Increases with hand grip and squatting

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27
Q

Characteristics of the holosystolic murmur in tricuspid regurgitation:

A

Best heard at the left 2 and 3 intercostal spaces

Increases with inspiration

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28
Q

Characteristics of the holosystolic murmur in ventricular septal defect:

A

Best heard at the left 3 and 4 intercostal spaces
Harsh, loud and accompanied by a thrill
Increases with hand grip

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29
Q

Which receptors are regulated by cortisol?

A

Cortisol upregulates α1 receptors of epinephrine (in blood vessels)

Also inhaled corticoids upregulate β2 receptors in bronchial smooth m. increasing responsiveness to albuterol. Also up regulates β receptors in the liver

Adequate cortisol levels allow glucagon to work releasing glucose

(Thyroid hormone upregulates beta 1 receptors of epinephrine (on the heart))

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30
Q

Which receptors are regulated by thyroid hormone?

A

Thyroid hormone upregulates beta 1 receptors of epinephrine (on the heart)

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31
Q

What accentuates the splitting of S2 in inspiration?

A

Conditions that delay RV emptying (pulmonic component) as pulmonary stenosis and right bundle block

Because inspiration delays the pulmonic component of S2

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32
Q

What causes a wide and fixed splitting of S2:

A

ASD
Accompanied with a mid-systolic ejection murmur on the pulmonic area (left upper) because causes RV overload! The murmur is systolic!

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33
Q

What is the paradoxic splitting of S2 and what causes it?

A

Splitting of S2 on expiration

Caused by conditions that make the aortic valve close very late as advanced aortic stenosis and left bundle block

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34
Q

Where in the airway is the biggest resistance and why?

A

In the SEGMENTAL bronchi, first and second divisions
due to turbulent flow

Segmental bronchi → Subsegmental bronchi → Terminal bronchioli* → Respiratory bronchioli
* Terminal bronchioles are the ones inflamed in asthma

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35
Q

Hyperkalemia consequences:

A 
Cell depolarization (chronic weakness and fatigue)
High T waves (V. fib)
Acidosis
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36
Q

Hypokalemia consequences:

A 
Cell hyperpolarization (weakness and fatigue)
Long QT (Torsades) and U waves
Decreased insulin secretion
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37
Q

Stimuli that increase vasopressin-ADH:

A

High osmolality: osmolality activates hypothalamic osmorreceptors

Low BP: low baroreceptor stretch activates the sympathetic but also ADH secretion

Stress: CRH and AT2 can increase ADH

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38
Q

Stimuli that increase aldosterone:

A

High ATII
High K

ACTH does not control aldo!

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39
Q

Stimuli that increase renin:

A

Low perfusion pressure to the kidney (~low BP)
Low Na to the macula densa*
High sympathetics to the kidney

*Low Na to the macula densa causes no Na to go into the macula densa trough Na/K/2C so no depolarization and no Ca influx which actually activates the Ca inhibited adenylate cyclase and increases renin release

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40
Q

Alpha 1 effects:

A

VasoCONSTRICTION

Smooth m. CONTRACTION (bladder sphincter, GU, pupillary dilator)

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41
Q

Alpha 2 effects:

A

Decrease sympathetic activation at the CNS
Inhibits insulin release and lipolysis
Decreases aqueous humor
Increases platelet aggregation

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42
Q

Beta 1 effects:

A

Heart: increase HR and contractility

Increase renin release in juxtaglomerular cells

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43
Q

Beta 2 effects:

A

Lungs: bronchodilation
Vessels: vasoDILATION
General smooth m. RELAXATION: uterus relaxation
Increases insulin (and K cellular uptake) release and lipolysis but alpha 2 effect is predominant
Decrease glucogenolysis (this is how β blockers cause hypoglycemia)
Increases aqueous humor

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44
Q

Bone remodeling indicators:

A

High serum osteocalcin and alkaline phosphatase

High urinary excretion of hydroxyproline

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45
Q

Which drug causes nephrogenic diabetes insipidus?

A

Lithium

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46
Q

LH acts on which cells:

A

Leydig cells in males and theca cells in females

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47
Q

FSH acts on which cells:

A

Sertoli cells in males and granulosa cells in females

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48
Q

Hormones inhibited by somatostatin (octreotide):

A 
Insulin
Glucagon
Gastrin
VIP
CCK
GH
TSH!!!

Somatostatin has 3 min half life but octreotide 90 min

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49
Q

Function of Apo B-48:

A

Transport chylomicrons out of the cell into the lymphatics

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50
Q

Function of Apo C-II:

A

Activates lipoprotein lipase that breaks down TG in the chylomicrons into FA so they go into the adipocyte

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51
Q

Function of Apo E:

A

For rEcycling chylomicron rEmnants and LDL

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52
Q

Which hypothalamic nucleus mediates satiation?

A

The ventromedial nucleus

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53
Q

Which hypothalamic nucleus mediates hunger?

A

The lateral nucleus

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54
Q

Key changes in neurogenic shock:

A

Vasodilation and no sympathetic activation

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55
Q

Key changes in septic shock:

A

Vasodilation and sympathetic activation (increase HR and contractility)

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56
Q

Key changes in hypovolemic shock:

A

Loss of fluid and vasoconstriction

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57
Q

Key changes in cardiogenic shock:

A

Left ventricular failure and vasoconstriction

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58
Q

What is the vital capacity?

A

Everything but the residual vol.

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59
Q

Which thyroid parameters increase in pregnancy?

A

You have more binding proteins! (even if you have less albumin causing edema)
T3 resin uptake is low
Just the TOTAL T3 and T4

The free ones and TSH are normal

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60
Q

Where do the curves for lung collapse tendency and chest expansion tendency meet?

A

At the functional residual capacity (increases in emphysema and decreases in fibrosis)

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61
Q

Hormones that bind intracellular receptors:

A 
Cortisol 
Estrogens
Progesterone
Testosterone 
Vit D
Aldosterone 
Thyroid hormone
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62
Q

Which 3 molecules can increase acid production by parietal cells?

A

Ach: blocks H/K and ↑ Gastrin
Gastrin: blocks H/K and ↑ His
Histamine: blocks H/K

But in general all 3 act synergistically so inhibiting one will decrease the effect of all of them. Omeprazol blocks all!

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63
Q

Hormones secreted by the posterior pituitary:

A

ADH

Oxytocin

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64
Q

The smooth endoplasmic reticulum is needed to and in which cells is big:

A

Make steroid hormones (androgens, estrogens, corticoids and aldo) and lipoproteins
Detoxify
Glycogen degradation and gluconeogenesis

Liver, adrenal cortex and gonads have big SER

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65
Q

The rough endoplasmic reticulum is needed to and in which cells is big:

A

Make secreted substances as peptide hormones (ADH, insulin, gastrin, PRL…)
Make lysosomal enzymes
Make membrane proteins

They are marked with the N-terminal hydrophobic sequence so they are recognized by SRP

Globet and plasma cells have big RER

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66
Q

What does extracellular Ca2+ to the fast Na+ ch?

A

High extracellular Ca2+ blocks fast Na+ ch

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67
Q

What K channel is deficient in congenital long QT segment? Where is the gene? What syndromes are generated?

A 
Delayed rectifier (one open in phase 2 and 3)
D3!

Chromosome 11

AR: Jervell Lange-Nielsen ❤️👂
AD: Romano-Ward ❤️

(also Na ch that take longer to close after action potential)

Do not give 1A and 3 antiarrhythmics! Give Mg if they get torsades

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68
Q

What is RANK-L’s function?

A

Differentiates osteoclasts, promotes bone break down

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69
Q

What is OPG’s (osteoprotegerin) function?

A

Prevents RANK-L to bind and activate osteoclasts

So decreases bone break down

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70
Q

What activates PTH and what are it’s functions?

A

Low Ca activates PTH and PTH increases Ca

By:
Activating Vit D
Decreasing renal Ca waste (and wasting K)
Breaking down bone (activates osteoblasts that activate osteoclasts in a paracrine way)

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71
Q

What activates calcitonin and what are it’s functions?

A

High Ca activates calcitonin and calcitonin stops bone break down

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72
Q

What activates Vit D and what are it’s functions?

A

Low Ca activates PTH and PTH activates Vit D, Vit increases Ca and bone

By:
Increasing Ca and P GI absorption (calbindin)
Enhancing PTH action on distal tubule

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73
Q

Manuvers that decrease the murmur in HOCM:

A

Manouvers that increase preload and/or afterload:
Passive leg raise
Hand gripping
Squatting

It is decreased by strain Valsalva

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74
Q

Changes in prerenal, renal and postrenal acute renal failure:

A

Pre: low FeNa high BUN

Renal: high FeNa low BUN

Postrenal:

early: low FeNa high BUN
late: high FeNa low BUN

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75
Q

Type of hypoxemia that cannot be corrected by 100% oxigen:

A

Right to left shunt!

Low PaO2, PARTIAL PRESSURE! that cannot be corrected

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76
Q

Pressure readings in RV, pulmonary artery and Wedge pressure:

A

RV: 0-25
Pulmonary A: 10-25
Wedge pressure: 5-10

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77
Q

Muscle spindles trigger, reflex involved and innervation:

A

Respond to muscle stretch: involved in myotactic reflex (patellar…)
Innervated by type 1a (and 2 neurons)

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78
Q

Golgi tendon organ trigger, reflex involved and innervation:

A

Respond to muscle force: involved in inverse stretch reflex in which muscle contraction is stopped during excessive stretch (too much weight)
Innervated by type 1b

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79
Q

Causes of metabolic acidosis with high anion gap:

A

MUD PILES

Methanol 👁: antidote is fomepizole/ethanol
UREMIA! 
Diabetic ketoacidosis 
Paracetamol
Iron!!! Isoniazid 
Lactic acidosis 
Ethylene glycol (antifreeze) nephrotoxic and oxalate crystals: antidote is fomepizole/ethanol
Salycates
  • Propylene glycol (antifreeze) also causes an anion gap metabolic acidosis and does not cause 👁 or kidney symptoms just seizure and coma
    • Isopropil alcohol (rubbing alcohol) does NOT cause an anion gap metabolic acidosis just coma

If no anion gap think about, bicarb loss: diarrhea, fistula, renal tubular acidosis (acetazolamide, spironolactone, addison), massive IV saline infusion that ↑ Cl, ingestion of HCl

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80
Q

What do you measure to diagnose 21–beta hydroxylase deficiency?

A

17-Hydroxyprogesterone

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81
Q

The Golgi apparatus is needed for which two functions?

A

Distribution
Post-transcriptional modification (for example phosphorylation of mannoses in lysosomal enzymes by phosphotransferase so they can enter the lysosomes)

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82
Q

N-glycosylation: what is it? Where? and what for?

A

Addition of sugars to asparagine
Stars in the ER can be modified in the Golgi for example by phosphorylation of mannoses in the N-linked sugars
Modify prot as for target them into heading to lysosomoes

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83
Q

O-glycosylation: what is it? Where? and what for?

A

Addition of sugars to serine and threonine
In the Golgi
Modify prot as for AOB blood groups

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84
Q

Thyroid panel in thyrotoxicosis facticia:

A

↓ TSH and ↓ RAIU (radioactive iodine uptake) ↓ thyroglobulin (T4 precursor)

If patient is taking:
T3 (triiodohyrosine): ↑ T3 (triiodohyrosine) only
T4 (thyroxine/levothyroxine): ↑ T4 and T3 (because T3 comes from T4 breakdown)

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85
Q

Respiratory changes with age:

A

Lung compliance increases (recoil loss=elastance loss)
Chest wall compliance decreases (stiff)
Chest wall becomes stiff and lungs fluffy
Residual vol increases

Other more predictable:
Increase: A-a gradient, V/Q mismatch
Decrease: FVC, FEV1, strength, cough, arterial PO2, ventilatory response to hypoxia and hypercapnia

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86
Q

Sertoli cells functions:

A 
Secrete inhibin B to inhibit FSH
Secrete androgen-biding protein
Convert testosterone to androstenedione
Secrete MIF
Support and blood testes barrier!!!
Temperature sensitive
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87
Q

Physiologic changes when you get into the water:

A

Blood vol increases
ANP increases
ADH decreases: pee

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88
Q

Which diseases produce dull and which ones hyperresonant percussion?

A

Dull:
Deceased fremitus: pleural effusion, atelectasis
Increased fremitus: pneumonia, pulmonary edema

Hyperresonant: pneumothorax

89
Q

In which disease do you get aldosterone escape?

A

In diseases with high aldo!

High aldo (Conn sd) doesn't cause hypernatremia due to aldosterone escape. You have HT and hypervolemia but you pee a lot because of the Aldo escape.
Low aldo does cause hyponatremia

Conn nr Na; only one where there is pressure natriuresis
Corticosteroid tto ↑ Na ↓ Ca
Addison ↓ Na

90
Q

NT changes in Parkinson:

A

DA is low

Ach is high (you treat with antimuscarinics at the beginning)

91
Q

What is the only nephron area with brush border microvilli?

A

Proximal convoluted tubule

Also the one that consumes the most ATP and the one affected in ATN

92
Q

Which hormone is responsible of controlling plasma Na concentration? Which hormone controlled the total Na?

A

Concentration: ADH. It does it within minutes
Total: RAAS

93
Q

What is the main cause of edema in pregnancy?

A

A fall in plasma oncotic pressure!!!

Increase in blood vol (1st change) causes hemodilution that causes a fall in plasma oncotic pressure (main contributor to the edema)

94
Q

What over and underestimates HbA1c?

A 
Overestimates: RBCs live longer because you cannot make more
Deficiencies: iron, B12, folate
Low EPO: renal failure
Marrow suppression: alcoholic
Splenectomy
Increased glycation: acid RBS

Underestimates: high RBCs breakdown (thalassemias…) or when you can make young ones
Supplements: iron, B12, folate
High EPO: doping, altitude
Splenomegaly
RA, reticulocytosis and liver disease
Drugs: antiretrovirals, ribavirin, antimalarials, dapsone
Decreased glycation: aspirin, vits C and E and basic RBC

95
Q

What is the sarcolemma?

A

The cell membrane of the myocyte

96
Q

What causes an increase in pulse pressure?

A

PP= SV/compliance
Aortic regurgitation (thoracic aortic aneurism)
Isolated systolic hypertension in elderly (↑ systolic is part of normal aging)
PDA
Transient in exercise (diastolic stays same)
Hyperthyroidism, anemia (hypoxia vasodilates), pregnancy
Obstructive sleep apnea
Aortic dissection
Lying down

97
Q

Substances that act in the afferent and efferent arteriole:

A

Afferent:
Dilate: PGs, DA, (ANP)
Constrict: sympathetics, adenosine, (AT2)

Efferent:
Constrict: AT2, ANP, (sympathetics)

98
Q

What is the enzyme that cleaves trypsinogen into trypsin?

A

Enterokinase or enteropeptidase

It is a brush border enzyme in duodenum and jejunum

99
Q

Which food can increase blood pressure de novo very fast?

A

Fructose is associated with initiation of metabolic sd. and HT. It increases production of uric acid that activates RAAS and vascular smooth m. proliferation

Na worsens HT in preexisting disease

100
Q

What causes a decrease in pulse pressure?

A

Cardiac tamponade
Cardiogenic shock
Advanced HF
Aortic stenosis

101
Q

What do the alpha and delta granules of the platelets contain?

A

alFa: vwF, Fibrinogen, Fibronectine, platelet Factor 4

Delta or dense: CASH: Calcium, Adp, Serotonin, Histamine

102
Q

Causes of hypoxemia:

A

V/Q mismatch with ↓ Q=Increase in death space: thrombus, pulmonary embolism (ends up diverting Q to other areas and therefore ↓V/Q)

V/Q mismatch with ↓ V: severe asthma, pneumonia, CF (partial). It’s extreme is shunt

R-L shunt: peanut (complete), atelectasis (ARDS, pneumothorax), congenital heart defects

Diffusion impairment: sarcoidosis, fibrosis, emphysema, pulmonary edema (left heart failure)

Hypoventilation: obesity, chest restriction (scoliosis), COPD, myasthenia gravis, opioids, altitude

103
Q

What do the different cells of the pancreas secrete?

A 
Alpha: Glucagon
Beta: Insulin
Gamma: Somatostatin
G: gastrin
Acinar: digestive enzymes
104
Q

What hormone is most elevated in PCOS?

A

LH, theca very sensitive to LH causes high androgens which on top increase LH secretion
FSH is suppressed

105
Q

Physiologic changes during pregnancy:

A

RAAS activation: (ovary and decidua release renin ↑ angiotensinogen) ↑ aldo
↑ CO, HR, preload, PP, RPFlow, systolic ejection murmur
Hemodilution ↓ Hematocrit and physiologic anemia ↓ viscosity ↑ EPO and ↑ RBC mass to compensate
Vasodilation so ↓ resistance (due to progesterone, relaxin and ↓ sensitivity to AT2 and NE) ↓ afterload
=CVP
↓ MAP because ↓ diastolic
↓ Femoral venous pressure

↑↑ GFR (relaxin→ mild proteinuria and glucosuria) causes ↓ Creatinin ↓ renal th for glucose. At the beginning is due to the ↑ RPFlow later is due to hemodilution ↓ Albumin concentration and plasma oncotic pressure (also causes edema)

↑ Clothing factors ↑ all but 13 and 2 (DVT, give heparin if no in labor)
↑ fibrinogen ↑ fibrin cloths ↓ fibrinolysis because of fibrinolysis inhibitors derived from the placenta (plasminogen activator inhibitor-1)
↑ protein C resistance and ↓ protein S amount
↑ Alkaline phosphatase (↑ cholesterol ↓ bile acid excretion)
↑ Thyroid binding proteins

Hyperventilation ↑ tidal (progesterone); mild respiratory alkalosis ↑ O2 ↓ CO2 ↓ bicarb; nr pH
↓ lung vol. because of uterus leads to dyspnea
Insulin resistance and lipolysis ↓ RV ↓ FRC

GERD, constipation, cholelithiasis and hemorrhoids (P relaxes LES, GI smooth m. and gallbladder and uterus increases vein pressure)

106
Q

Aldo, K and Na levels in rhabdomyolysis:

A

Muscle breakdown releases myoglobin, K and creatine kinase

↑K causes ↑Aldo that causes ↑Na reabsorption and ↑K secretion

107
Q

Hormones that affect tubular transport and their effects:

A

PTH:
Inhibits P reabsorption at the PCT
↑Ca reabsorption at the DCT by ↑TRV5 and NCX1

AT2:
↑H excretion at the PCT by activating NHE3

ADH:
↑NaCl reabsorption at the ascending loop by activating NKCC
↑water reabsorption at the CD by ↑AQP1 and 2

Ca:
↓Ca reabsorption at the ascending loop by inhibiting NKCC

Aldo:
↑Na reabsorption and ↑K secretion at the CD by activating Na/K ATPase, ENaC and ROMK

108
Q

Physiologic changes in anemia:

A

↓ viscosity
↓ tissue O2 tension

↑ pulse pressure:
↑ systolic: ↑ CO, HR, contractility, EF, fluid retention over time
↓ diastolic: VASODILATION!!! so ↓ resistance ↑ venous return but ↓ splanchnic blood flow

109
Q

Types of AV block:

A

R is far from P you have a first degree, PR>200
Longer, longer drop you have Mobitz 1 (Wenckebach)
Some Ps don’t go trough you have Mobitz 2
R and Ps don’t agree you have a 3rd degree

110
Q

What causes hyperglycemia in DM1?

A

No insulin prevents uptake of glucose by muscle and adipose tissue through GLUT 4, they are the only insulin-dependent, the rest can take glucose with no insulin!

111
Q

What is renal threshold for glucose?

A

180-200; glucose starts appearing in urine
375 is transport maximum (any extra glucose will go to the urine)
↑GFR ↓thresholds and vice versa
Chronic hyperglycemia ↑glucose threshold

112
Q

Which cells secrete colecystokinin, GIP and Somatostatin?

A

Colecystokinin: I cells
GIP, GLP-1: K cells
Somatostatin: D cells

113
Q

Where are Ach, DA, GABA, NE and 5-HT synthesized?

A

Ach: Meynert
DA: Ventral tegmentum and substantia nigra compacta
GABA: Acumbens
NE: Locus ceruleus (hypersensitivity in panic disorder)
5-HT: Raphe

114
Q

Receptors coupled to Gq (IP3, DAG system) and what do they cause?

A 
HαV An MandM
H1: histamine, allergy, alertness, vomiting
α1: NE and epi, vasoconstriction
V1: ADH, vasoconstriction
AT1: AT2, vasoconstriction
M1: Ach, activates CNS
M3: Ach, leaky

Also gastrin, OXYTOCIN, GnRH, TRH

115
Q

Receptors coupled to Gs (↑ cAMP system) and what do they cause?

A

β1: NE and epi, activates heart
β2: epi, relaxation (lung, uterus) and ↑insulin
β3: epi, relaxation (bladder)
D1: DA, vasodilation and activates basal ganglia
H2: histamine, gastric acid
V2: ADH, aquaporins and vW and F8 release

116
Q

Receptors coupled to Gi (↓ cAMP system) and what do they cause?

A

MAD2
M2: Ach, relaxes heart
α2: NE and epi, ↓insulin
D2: DA, inhibits basal ganglia

117
Q

What helps maintain CO in hemorrhage?
What helps maintain blood volume in acute hemorrhage?
What helps maintain blood pressure in hemorrhage?

A

CO: venules and veins contriction; because they normally accommodate a lot of blood (reservoir) Sympathetic stimulation causes venoconstriction!

Volume: recruitment of fluid form the interstitium, happens passively and fast

Pressure: arteriolar constriction, ↑SVR

CO-Veins
Vol-Intertitium
Press-Arterioles

118
Q

Causes of increased vascular permeability:

A

Infections
Toxins (gram - sepsis)
Burns
ARDS

119
Q

What indicates high severity in mitral stenosis? and in mitral regurgitation?

A

In mitral stenosis ↓ between S2 and the opening snap

In mitral regurgitation S3

120
Q

Which organs help the body heal after injury and handle infections?

A

Adrenal CORTEX

Thyroid (a lot of undiagnosed hypothyroidism in elderly)

121
Q

Which part of the nephron have the lowest pH and therefore most stones form there?

A

Distal tubule and collecting duct

122
Q

Regions where urine is most concentrated and diluted in ADH absence and presence of ADH:

A

Drinking and peeing, ↓ ADH:
Most concentrated, highest osmolality: Junction between ascending and descending loop of Henle

Most diluted, lowest osmolality: Collecting duct

Dehydrated, ↑ ADH:
Most concentrated: Collecting duct will become the most concentrated because water goes to the blood (~Henle junction)

Most diluted: DCT

123
Q

Function of Apo A-I:

A

Activates LCAT, found only in HDL

124
Q

Which O2 parameter remains constant on CO poisoning, methemoglobinemia, anemia and polycythemia? Which one changes?

A

Remains constant: PaO2, PARTIAL PRESSURE! of O2 or dissolved O2 (P50 will be nr in anemia and polycytemia and ↓ in CO and methemoglobinemia)

Changes: O2 content or total O2!

Normal partial pressure low content

  • In CO poisoning and methemoglobinemia ↓O2 saturation in anemia ↓Hb concentration
125
Q

Which 2 parts of the kidney are never permeable to water?

A

Ascending limb of the loop of Henle

Distal convoluted tubule

126
Q

Which is the only ion that influences resting membrane potential?

A

K

127
Q

Causes of hyponatremia:

A 
SIADH: small cell lung ca, pneumonia, CNS trauma, stroke or hemorrhage, carbamezapine, SSRIs and NSAIDs
Primary polydipsia
Marathon runner that is drinking a lot (stress ↑ ADH)
Inadequate Na intake in alcoholics
Saline infussion
Diuretic use
Hypoadrenalism
Hypothyroidism!!!
128
Q

DD of nonpitting edema:

A 
Lymphatic obstruction (Wuchereria bancrofti)
Thyroid myxedema
129
Q

Leukocytes physiologic values:

A 
Never Let Monkeys Eat Bananas:
All leukocytes: less than 11k
Neutrophils ~ 70%
Lymphocytes ~ 30%
Monocytes < 10%
Eosinophils < 5%
Basophils  < 2%
130
Q

Which hormone causes morning sickness?

A

Beta HCG

In mole is very high so those patients have hyperemesis and even projectile vomiting

131
Q

Does an increase in preload increase the systolic interval?

A

No, it does not increase or decrease the systolic interval (time spent in contraction)

Both preload (by Frank-starling) and contractility increase the force of contraction but only contractility affects the systolic interval

132
Q

What happens right after you inject insulin on a healthy patient?

A

Hypoglycemia. The body will try to compensate! by increasing glucagon (even if in normal physiology insulin suppresses glucagon), GH and epi

133
Q

If alkaline phosphatase is low, how is PTH?

A

If alkaline phosphatase is low PTH is low because PTH breaks down bone by activating osteoblasts to release RANK-L

134
Q

What does a decrease in Ca, K, and Mg do to the QT interval?

A

Low Ca, K, and Mg delay the opening of the K rectifier and therefore prolong QT

High Ca causes a short QT

135
Q

Juxtaglomerular apparatus composition:

A

Macula densa: tall cells in the distal convoluted tubule that monitor urine salt content by the Na/K/2Cl ch and send info to the JC cells. *Low Na delivery to the macula densa causes no Na to go into the macula densa trough Na/K/2C so no depolarization and no Ca influx which actually activates the Ca inhibited adenylate cyclase and increases renin release

Juxtaglomerular cells (in the cortex): modified smooth muscle cells on afferent arteriole that sense pressure → release renin

Extraglomerular mesangial cells: Lacis cells

136
Q

What is the low urine specific gravity and osmolarity (dilated)? What is high (concentrated)?

A

Low:
Specific gravity less than 1.010
Osmolarity less than 200

High:
Specific gravity more than 1.015
Osmolarity more than 450

137
Q

What is the dx if O2 therapy does not correct hypoxemia?

A

Pulmonary shunt

138
Q

How is hemithorax volume in pneumothorax compared to normal lung?

A

Increased, because of loss of IPP the chest wall springs out of the equilibrium position

139
Q

How are ADH, NE and Epi in Addison disease?

A

↑ ADH, compensates for hypovolemia
↓ Epi because cortisol is needed to convert NE in Epi
↑ NE, compensatory

140
Q

EKC effects of class 1,2,3 and 4 antiarrhythmics:

A

1: Na ch block: prolong QRS!!!!
2: Beta block: slow HR and prolong PR
3: K ch block: prolong QT
4: L-Ca ch block: slow HR and prolong PR
1,3,4: increase effective refractory period

141
Q

What is the function of the acinar and ductal cells in saliva production?

A

Acinar cells secrete initial saliva, isotonic

Ductal cells modify initial saliva, causing reabsorption of NaCl and secretion of K and Bicarb, becomes hypotonic

Ductal reabsorption happens more if there at low-flow rates so the saliva becomes more hypotonic; at high-flow rates becomes more isotonic

142
Q

Metabolic panel in iron overdose:

A

Early: Abdominal pain that can lead to bowel obstruction weeks later

Late: Anion gap metabolic acidosis without tachypnea
Also, normal Na, K and Cl!
Respiratory failure
Coagulopathy

143
Q

How is total renal function affected after total nephrectomy?

A

Right after the sx 50% decrease in function, weeks later just 75-80% decrease in function

144
Q

What does Cr do to GFR estimation? Why?

A

OVERestimates GFR
Because it is SECRETED
The SECREt of Cr is that she is HIGH form weed!

145
Q

Which hormone accelerates gastric emptying?

A

Gastrin

146
Q

Physiologic changes in mild hypothermia:

A

Sympathetic activation
Shivering: involuntary muscle contractions (main mechanism to maintain temperature initiated in the posterior hypothalamus)
Peripheral vasoconstriction causing ventral hypervolemia
ADH decreases: pee (Gauer-Henry reflex)

147
Q

Metabolic panel in vomiting:

A

Metabolic alkalosis with low urinary Cl
↓ Na, K, H, Cl
↑ Bicarb (contraction alkalosis because of ↑AT2 that ↑ Na/H exchange int he PCT and ↑aldo that ↑ H secretion by α-intercalated cells)

148
Q

Metabolic panel in diarrhea; how do you treat it?

A

No anion gap metabolic acidosis
↓ K, Na and bicarb. Worry about hypoNatremia if just drinking water especially if baby → seizures. But worry about hypoKalemia with laxative abuse
↑Cl (compensation for ↓ bicarb)
Give glucose and salt because glucose is co-transported into enterocytes via Na

149
Q

If which pathology corresponds to LV systolic pressure bigger than aortic systolic pressure?

A

Aortic stenosis

150
Q

What is a normoblast?

A

Immature RBC, stimulated by EPO

RBC precursors contain ribosomal RNA still remaining from development that can be seen with methylene blue staining or Wright stains

151
Q

Which cell proliferates during pregnancy causing pituitary enlargement?

A

Lactotropes

152
Q

What is the effect of thyroid hormone in the bone?

A

T3 increases bone resorption

In hyperthyroidism PTH will be ↓↓↓ but Ca in plasma will be normal

153
Q

What are the key differences between hypertrophic cardiomyopathy and aortic stenosis murmurs?

A

Same:
Systolic on the right upper sternal border
Decrease with hand grip (↑ afterload only). If ↑ it is VSD, AR or MR

Different:
Hypertrophic ↑ with Valsalva
AS ↓ with Valsalva (as most murmurs)

154
Q

Hemodynamic changes secondary to PDA and AV fistula:

A

↑CO ↑HR ↑SV; CO increases in a L to R shunt!!! as in PDA or AV fistula; can end up in high output heart failure
RAAS activation and vol. overload because the kidney senses the ↓TPR
↓Afterload (arterioles are a major source of resistance so bypassing the arterioles results in a decrease in ↓TPR)
= systemic O2

155
Q

Which hormones are secreted in the duodenum?

A

CCK (I cells)
GIP (K cells)
Secretin (S cells)

156
Q

Hemodynamic changes secondary to VSD:

A

L to R shunt!!!
Pressure in the RV is going to increase and actually pulmonary pressure and LA pressure are going to increase too
LV pressure is variable
RA pressure is normal

If R to L shunt is just the inverse

157
Q

Thyroid panel in thyroid hormone resistance vs in ↑ thyroid biding globulin:

A

Thyroid hormone resistance:
Clinically hyperthyroid, normally in a hyperactive kid
↑T4, T3 and TSH
Mutation in the thyroid hormone receptor β (T4 and T3 are not inhibiting TSH secretion)

↑Thyroid biding globulin:
Clinically euthyroid in pregnant or woman on contraceptives
nr free T4, T3 and TSH
↑ total T4, T3

158
Q

Calcium panel in familial hypocalciuric hypercalcemia vs in pseudohypoparathyroidism:

A

Both are autosomal dominant

Familial hypocalciuric hypercalcemia (calcium resistance):
CaSRs (Gq) do not work. They normally will inhibit PTH release form the parathyroid and excrete Ca in the kidney
↑ Ca and PTH in plasma
↓ Ca in urine
Cincalcet sensitizes CaSRs in the parathyroid and is used to treat hyperparathyroidism in kidney failure

(Different form AD hypocalcemia where CaSRs overworks so you have ↓ Ca, PTH and ↑ P in plasma)

Pseudohypoparathyroidism (PTH resistance):
GNAS1 (Gs) do not work. They normally break down bone and eliminate P
Adynamic bone disease
↑ P and PTH in plasma
↓ Ca in plasma

159
Q

What does EF measures?

A

Contractility

160
Q

Which kind of proteins do free and attached ribosomes synthesize?

A

Free: cytosolic, nucleosolic, peroxisomal and mitochondrial proteins

Attached: secretory, cell membranes (both nuclear ande cytoplasmic), ER, Golgi and lysosomal proteins

161
Q

Thyroid panel in de Queravin and Hashimoto vs Graves:

A

De Queravin and Hashimoto:
HYPER: ↑T4, ↑T3, ↑plasma thyroglobulin*, ↓TSH, ↓uptake**
HYPO: ↓T4, ↓T3, ↑TSH (goiter and ↑uptake**)

Graves: HYPER: ↑T4, ↑T3, ↑plasma thyroglobulin*, ↓TSH (but IgG act as TSH: goiter and ↑uptake**)

  • plasma thyroglobulin is normally equivalent to plasma T4, the only time you get ↑T4 with ↓plasma thyroglobulin is due to exogenous (is like C-peptide)
    • uptake and goiter normally increase or decrease based on TSH receptor activation. If doubt in De Queravin and Hashimoto uptake is ↓
162
Q

DD. of undetected PDA vs aortic coarctation:

A

Undetected PDA: BLUE
PDA stays open:
Continuous machine-like murmur at the left infraclavicular area
Bounding pulses (as in AR) because of the L→R shunt there is increased LV preload so ↑systolic; and because the flow gets lost into the R circulation ↓diastolic
L→R shunt at the beginning but the R❤️ and lungs get a lot of pressure so ↑pulmonary flux can develop R❤️failure. Then R→L shunt so lower body CYANOSIS
No coarctation: no weird pulses, just BLUE!

Coarctation; POSTductal: NO LOWER PULSES
Coarctation: bounding PULSES (↑TPR) JUST in upper body and NO PULSES (↓BP) in lower body
Systolic ejection murmur or even continuous murmur ON THE BACK ±S4
Because of the upper body ↑TPR can lead to L❤️ failure, aortic dissection, stroke, endocarditis, endarteritis…
No shunt: same flow through all circuit
PDA closes: no machine-like murmur and not blue, just ABSEBT PULSES
No cyanosis because tissues autoregulate their blood flow Q=P/R

Both present very similarly: teenager with leg cramps

Coarctation; PREductal: mixture
Very different for the other 2: half blue baby associated with turner
Coarctation: bounding PULSES in upper body and NO PULSES in lower body
+
PDA stays open:
Continuous machine-like murmur
Also contributing to the bounding pulses in the upper body, if closes baby goes into shock
R→L shunt because of the low aortic pressure: lower body CYANOSIS

Coarctations are associated with bicuspid aortic valve and intracranial aneurisms and Rx 3 sign

163
Q

What murmur do you hear in ASD?

A

Mid-systolic on the pulmonic area (left upper sternal border)

164
Q

Beneficial effects of mechanical ventilation in the treatment of ARDS:

A 
ARDS= diffuse alveolar damage
↑ FRC
Prevent alveolar collapse
↓ Tidal vol. prevents barotrauma
In PEEP all pressures become positive!
165
Q

What is the cause of the hypoxemia in pneumonia?

A

V/Q mismatch

166
Q

What is the cause of the hypoxemia in pulmonary embolism? What is the metabolic panel?

A

V/Q mismatch

↓Oxygen and acute respiratory alkalosis due to hyperventilation

167
Q

What is the cause of the hypoxemia in pulmonary edema? What happens with compliance?

A

Diffusion impairment
There is also V/Q mismatch because of low ventilation (similar to pneumonia)
Compliance ↓

168
Q

Which 2 vitamins increase due to bacterial overgrowth and decrease due to antibiotics?

A

Vit K and FOLATE

169
Q

What should you think if you hear a systolic murmur on the left 2nd intercostal space on an athlete?

A

It is most likely a pulmonic flow murmur, it is a normal finding due to high SV on an endurance athlete

170
Q

What is the function of enteropeptidase?

A

Activate trypsinogen to trypsin

171
Q

What are the changes on the affected and non-affected kidney in renal A. stenosis?

A

Affected:
↑ renin release
NEAR NORMAL GFR!!! due to tubuloglomerular feedback but ↓FLOW AND ↑FF
↑ Na and water reabsorption due to AT2 and Aldo
Afferent dilation+efferent constriction which contributes to =GFR

Non-affected:
↑ Na excretion due to pressure natriuresis
↑ Arteriolar wall thickness (hypertensive nephrosclerosis)

Peripheral:
↑TPR due to AT2

172
Q

How does hyperthyroidism cause osteoporosis?

A

Activates osteoclasts that break down bone

173
Q

How is TPR in PDA? Why?

A

In PDA you have a L to R shunt so the TPR decreases because there is one more way that the blood can follow when it comes out the LV

174
Q

Key associations for Bohr and Haldane effects:

A

Bohr: tissues, venous, ↑H+*, curve shifts right, gives O2 away (UNloaging), CO2 enters the RBC and makes bicarb so the bicarb that is made is taken out of the RBC in exchange with Cl ↑Cl in the RBC
*Deoxygenated blood carries a lot of CO2 that makes H+ and bicarb, the more deoxygenated the blood the more CO2 will be attracted into the RBC

Haldane: lungs, arterial, ↓H+, curve shifts to left, takes O2, kicks out CO2, bicarb goes into the RBC to make more CO2 and kicks it out. Bicarb goes inside in exchange with Cl so ↓Cl in the RBC

The majority of CO2 is transported as bicarb in plasma

175
Q

How are Cr clearance and PAH clearance correlate with the parameter than they estimate?

A

Cr clearance OVERestimates GFR because a little is secreted, real GFR is 20% less

PAH clearance UNDERestimates RPF because a little cannot be secreted, real RPF is 20% more. It is more underestimated as [PAH]↑ because more stays in the blood

176
Q

What causes the dynamic LV outflow tract obstruction in HOCM?

A

Mitral valve (anterior leaflet) moves towards interventricular septum

177
Q

What are the 3 functions of thyroid peroxidase?

A

OOKi
Oxidation: of iodiDe into iodiNe
Organification= Iodination of tyrosyl residues to make MIT and DIT
Coupling: of MIT and DIT into T3 and T4

178
Q

How do high and low flow affect saliva and pancreatic exocrine concentrations?

A

Saliva:
Low flow: more reabsorption; hypotonic; ↓Na ↓Cl ↑bicarb ↑K
High flow: less reabsorption; isotonic; ↑Na ↑Cl ↓bicarb ↓K
Acinar cells secrete initial saliva, isotonic

Pancreas exocrine:
Low flow: ↓bicarb ↑Cl, like in plasma
High flow: ↑bicarb ↓Cl
Na and K do not change so it is always isotonic

179
Q

Main changes of O2 parameters on CO poisoning and methemoglobinemia? Which 3 parameters remain constant?

A 
↓ O2 carrying capacity
↓ O2 content or total O2
↓ P50
LEFT shift
Note that cyanide does not affect O2 dissociation at all

CONSTANT:
PaO2
PARTIAL PRESSURE of O2
Dissolved O2

180
Q

Changes in the O2 dissociation curve in high altitude:

A

RIGHT shift
↑2,3-BPG (takes a little time)
↓PaCO2

181
Q

Does glucose enter the pancreas in. hypoglycemia?

A

Yes
GLUT2 are insulin-INdependent, glucose will be able to enter the beta-cells of the pancreas and the liver
*It is bidirectional

182
Q

Changes caused by pathologies in jugular venous pulse:

A

a wave: disappears in A fib, becomes huge in tricuspid stenosis, RHF and pulmonary HT, cannon a waves appear on AV dissociation and V-tach (giant a waves in just some cycles ↓LVEDiastolicV)

x descent and v wave: disappear in tricuspid regurgitation and right HF

y descent: big descent in constrictive pericarditis and not descent in tamponade

  • Everything said about the tricuspid valve and the RH applies to the mitral and LH too
183
Q

Metabolic panel in SIADH:

A

↓ plasma Na, osmolarity, uric acid and urea

nr K because Aldo is nr

184
Q

Which hormone stimulates the synthesis of Estrogens?

A

FSH
LH stimulates desmolase that induces the production of androgens by theca cells and then FSH stimulates aromatase that converts androstenedione to estrogens

185
Q

What do acidophils, basophils, amphophils and oxyphils secrete?

A

Acidophils, anterior pituitary: PRL
Basophils, anterior pituitary: FSH, LH, ACTH and TSH
Amphophils, anterior and intermediate pituitary: nothing
Oxyphils, parathyroid gland: PTH

186
Q

How does hypertension affect the number of arterioles?

A

Decreases arterioles number, because chronic vasoconstriction is followed by arteriolar disassembly

187
Q

Which hormone maintains the corpus luteum during pregnancy?

A

hCG

188
Q

Which hormone promotes rupture of the ovarian follicle during ovulation?

A

LH

To induce ovulation you can give recombinant hCG as if it was LH because it shares the alpha subunit with LH!

189
Q

What is one of the main functions of beta 3 receptors?

A

They are in brown fat and is the way that the sympathetic activates thermogenesis

190
Q

How do high and low dose dexamethasone suppress a cortisol secreting adrenal tumor?

A

None of them suppresses it

191
Q

Which are the most important chemoreceptors to monitor changes in lung function? and in COPD?

A

CENTRAL chemoreceptors in the medulla that sense CO2 directly and pH indirectly

In COPD the central chemoreceptors are adapted and the PERIPHERAL sensing O2 become the major respiratory drive

192
Q

Why does pressure back up backwards and not forward on the circulation?

A

Because of precapillary resistance, because of the arterioles

It backs up backwards because there is not a strong post capillary resistance and therefore venous pressure=capillary pressure

193
Q

Does ECV increase in burn patients?

A

No
The ECV consists of two compartments, the interstitial space and the intravascular space. In burn patients fluid moves out of the blood vessels into the interstitium (which decreases the intravascular volume and can lead to hypovolemic shock). So even though burn patients may have edema, there is no actual increase in the total content of fluid in the ECV! It just moves from one of its compartments into the next

194
Q

What makes a patient to have an altered consciousness in diabetic ketoacidosis?

A

Dehydration, intracellular and extracellular. That is why you give IV fluids

195
Q

Metabolic panel in pneumothorax and PE:

A

Hypoxemia and hyperventilation, so normally causes respiratory alkalosis because CO2 decreases

If the hyperventilation is not enough CO2 accumulation can lead to respiratory acidosis

196
Q

How is pulmonary vascular resistance in a MI pulmonary edema?

A

Decreased
More blood in pulmonary vasculature → the capillaries will dilate in order to keep all these blood → decreased pulmonary vascular resistance

197
Q

Why after you remove a cuff you get vasodilation? what else do you get in ischemia?

A

Because of adenosine!
In ischemia you also get ↑K because the Na/K ATPase stops working and ↓Na Ca and bicarb. Ca accumulates inside the cytoplasm in cell injury

When they are talking about vasodilation in the cortex of ischemia (cuff/MI) think ADENOSINE and other metabolites
After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP and making ADP, but no fresh blood will be delivered so ADP accumulates making ADENOSINE that drives vasodilation of arteries!

198
Q

What is calcitriol?

A

The active form of vitamin D

199
Q

What is the most important metabolic imbalance consequence of hypothyroidism?

A

↓Na due to ↑ADH (SIADH)

200
Q

How do you differentiate between euthyroid sick syndrome and central hypothyroidism?

A 
Check the reverse T3
Euthyroid sick syndrome
↓ TSH, T4, T3 ↑rT3
Central hypothyroidism
↓ TSH, T4, T3, rT3
201
Q

Which congenital adrenal hyperplasia can be diagnosed in puberty?

A

17 alpha hydroxyls deficiency
Is a teenager that doesn’t menstruate
The hypertension and ↓K are normally mild and discovered on further checkup

202
Q

Which enzyme is blocked by ketokonazol?

A

Cholesterol desmolase: ↓ cortisol and treats Cushing; desolate is activated by LH in females
17,20 lyase: ↓ androgens so gynecomastia

203
Q

Which type of antibodies are seen in Addison’s?

A

Antibodies to 21-hydrosylase

204
Q

Where does HbA non-enzymatic glycosylation happen?

A

Valines on the beta chain of hemoglobin

205
Q

Why DM1 can cause muscle, respiratory and heart failure? and why does it cause cognitive problems?

A

Muscle problems: ↓Phosphate (acidosis takes P out of the cell and you pee it out) this affects the muscle

Cognitive problems: dehydration

206
Q

Which enzyme deficiency has a baby girl that virilizes at puberty?

A

XY with 5 alpha reductase deficiency

207
Q

What metabolic ph change is associated with hypercalcemia?

A

Acidosis
↑ Ca ↑ H

Ca also causes diabetes insipidus

208
Q

How do you know if a non-anion gap metabolic acidosis is due to renal losses or not?

A

Measuring the urine anion gap: Na+K-Cl
Positive, also if Na in urine is equal or more than 20 → renal losses as in RTA
Negative, also if Na in urine is LESS than 20 → diarrhea

Small Na in urine means you are loosing Na somewhere else

209
Q

What is fetal Hb made of?

A

α2γ2 gamma!!!!

210
Q

Which hormones accelerate and slow gastric emptying? Which ones increase and decrease gastric acid secretion ?

A

Accelerate and increase secretions:
Gastrin
(His and Ach just increase the secretions)

Slow and decrease the secretions:
Secretin
GLP, GIP
CCK

VIP just slows down
Somatostatin just decreases the secretions but it is the most important in decreasing them!

211
Q

What is the cause of the hypoxemia in ARDS? and in pneumonia?

A

Shunt due to non ventilated alveoli, the alveoli get blood but are not ventilated because they are full of water

Pneumonia is a V/Q mismatch because the no ventilation just happens in one are of the lung (ARDS is like a pneumonia un all the lung)

212
Q

What is the effect of Metyrapone and what is it used for?

A

It inhibits 11ß hydroxylase, so prevents the conversion of 11-deoxycortisol to cortisol so cortisol ↓ and this causes ACTH ↑. Same happens if you eat licorice

The opposite of dexamethasone that ↓ ACTH

  • the failure of both ACTH and 11-deoxycortisol levels to rise after the administration of metyrapone indicates secondary or tertiary adrenal insufficiency
213
Q

Causes of low anion gap:

A

Hypoalbuminemia
Multiple myeloma

Albumin is an important component of the anion gap

214
Q

What are the effects of hypermagnesemia?

A

Mg blocks Ca and K so it causes the same effects as low Ca and K

215
Q

Where does homologous recombination happen?

A

Prophase 1

216
Q

In which point of the cardiac cycle you get the peak coronary flow?

A

During diastole actually during the aortic notch, is when the pressure differential between the aorta and the left ventricle is the greatest
External compression of the coronary vessels by myocardial tissue results in paradoxical peak flow!

217
Q

When do you use dexamethasone suppression test and when ACTH suppression test?

A

Dexamethasone suppression test is used to diagnose the cause of INCREASED cortisol

ACTH suppression test is used to diagnose the cause of DECREASED cortisol
If ACTH ↑ cortisol: pituitary insufficiency
If ACTH ↓ cortisol: adrenal insufficiency

218
Q

Main metabolic abnormality in aldosterone and cortisol deficit:

A

Aldosterone deficit: hyperkalemia; Na is normal because of the Na escape
Cortisol deficit: hyponatremia because cortisol should inhibit ADH and here it cannot so there is ↑ADH; K is normal because Aldo is normal

219
Q

Functions of thyroid peroxidase

A

OOK:
Oxidation
Iodination=organification
Koupling

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