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Physiology Brs > Physiology Brs > Flashcards

Physiology Brs Flashcards

0
Q

Solution 150mM NaCl is …tonic

A

Isotonic

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1
Q

Solution 300mM mannitol is …tonic

A

Isotonic

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2
Q

At the muscle end plate ACh causes the opening of

A

Na and K channels

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3
Q

At the muscle end plate ACh causes …polarization to which value

A

Depolarization to a value halfway the Na and K equilibrium potentials

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4
Q

Why hyperkalemia causes muscle weakness?

A

Because Na channels are closed by depolarization

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5
Q

Function of γ-motoneurons

A

Innervate intrafusal myscle fibers –> adjust the sensitivity of the muscle spidle so that it will respond appropriately during muscle contraction

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6
Q

Decerebrate rigidity is caused by

A

Increased reflex muscle spindle activity due to removal of inhibition of higher centers

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7
Q

What kind of lesions cause decerebrate rigidity?

A

Lesions above the lateral vestibular nucleus and lesions above the pontine reticular formation but below the midbrain

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8
Q

The excessive muscle tone in decerebrate rigidity can be reversed by

A

Cutting the dorsal roots

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9
Q

Second order neurons in the olfactory pathway

A

Mitral cells

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10
Q

Low doses of epinephrine cause vasodilation/vasoconstriction?

A

Vasodilation (β2 more sensitive to epinephrine than α)

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11
Q

High doses of epinephrine cause vasodilation/vasoconstriction?

A

Vasoconstriction (μαλλον εχουν περισσοτερους α)

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12
Q

Conscious proprioception (below the lesion) after complete transection of the spinal cord

A

Permanently lost (because of the interruption of sensory fibers)

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13
Q

Stretch reflexes (below the lesion) after complete transection of the spinal cord

A

Temporarily lost (because of the spinal shock) , return with time or become hypersensitive

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14
Q

Dihydropyridine receptors (heart)

A

Voltage-sensitive protein of the T tubules, L-type channels. During the plateau of the action potential Ca2+ enters the cells from extracellular fluid through these channels

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15
Q

Ryanodine receptors (heart)

A

Ca2+ that enters the cell through the L-type channels (dihydropyridine receptors) triggers release of Ca2+ from the SR = Ca2+ -induced Ca2+ release)

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16
Q

Digitalis

A

Inhibits Na-K ATPase -> diminishes Na gradient -> diminishes Na-Ca exchange (that extrudes Ca) -> ^ intrac Ca

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17
Q

Pulmonary blood flow greater than aortic blood flow

A

Left-to-right ventricular shunt

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18
Q

A pattern of two P waves preceding each QRS complex indicates

A

Decreased conduction velocity in the AV node

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19
Q

The greatest pressure decrease in the circulation occurs across ______
because

A

Across the arterioles because they have the greatest resistance (ΔP= Q x R)

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20
Q

Cushing reaction

A

=response to cerebral ischemia.
^ intracranial pressure ->
compression of the cerebral blood vessels ->
cerebral ischemia (^ CO2) ->
sympathetic outflow to the heart and blood vessels ->
PROFOUND INCREASE IN ARTERIAL PRESSURE

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21
Q

Hering-Breuer reflex

A

Lung stretch receptors: distention of the lungs –> reflex decrease in RR

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22
Q

J (juxtacapillary) receptors

A

in the alveolar walls, close to the capillaries

Engorgement of the pulmonary capillaries (e.g. left heart failure) –> rapid, shallow breathing

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23
Q

Adaptation to high altitude

A
  • respiratory alkalosis (acetazolamide)
  • ^ EPO
  • ^ 2,3-DPG
  • Pulmonary vasoconstriction (hypertrophy if the right ventricle)
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24
Q

Mature levels of surfactant (can be reflected)

A

Lecithin:sphingomyelin ratio greater than 2:1

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25
Q

Major site of airway resistance in the lungs

A

Medium-sized bronchi

The smallest airways would seem to offer the highest resistance BUT parallel arrangement

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26
Q

Bohr effect

A

Increases in Pco2 / decreases in pH shift the curve to the right (e.g. during exercise: tissues produce more CO2)

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27
Q

Hemoglobin- O2 dissociation curve:

Shifts to the right

A
  • increases in Pco2/decreases in pH
  • increases in temperature
  • increases in 2,3-DPG concentration
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28
Q

Hemoglobin- O2 dissociation curve:

Shifts to the left

A
  • decreased Pco2/increased pH
  • decreased temperature
  • decreased 2,3-DPG (e.g. HbF)
  • CO poisoning
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29
Q

Cause of hypoxemia

A
  • decreased PAo2
  • diffusion defect
  • V/Q defects
  • right-to-left shunts
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30
Q

Abnormal A-a gradient

A 
>10mm Hg
Causes:
-diffusion defect
-V/Q defects
-right-to-left shunts
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31
Q

Causes of Hypoxia

A
  • decreased cardiac output / blood flow
  • hypoxemia
  • anemia (decreased hemoglobin concentration)
  • CO poisoning
  • Cyanide poisoning
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32
Q

Pulmonary blood flow greater than aortic blood flow

A

Left-to-right shunt:
In normal adults,output of left ventricle=output of right ventricle. When defect in ventricular septum (left-to-right shunt) the “shunted” fraction of the left ventricular output is added to output of the right ventricle

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33
Q

Chemoreceptors in control of breathing

A
  • CENTRAL
    • Medulla : pH
  • PERIPHERAL
    • Carotid bodies : Po2 (if <60mm Hg) , Pco2
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34
Q

NH3 synthesis in acidosis

A

Adaptive increase in NH3 synthesis
(in the renal cells –> diffuses down its concentration gradient from the cells into the lumen –> combines with H+ to form NH4+ –> NH4+ is excreted)

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35
Q

TBW is highest in

A

Newborns and adult males

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36
Q

TBW is lowest in

A

Adult females and in adults with a large amount of adipose tissue

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37
Q

Major ions of ICF

A

Cations: K+ and Mg2+
Anions: protein and organic phosphates (ATP,ADP,AMP)

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38
Q

Substances with the lowest clearances

A
  • not filtered: protein

- reabsorbed: Na+, glucose, amino acids, HCO3-, Cl-

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39
Q

Major ions of ECF

A

Cations: Na+
Anions: Cl- and HCO3-

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40
Q

Measuring the volumes of the fluid compartments-Markers

A
  • Tritiated water: for TBW (wherever water is found)
  • Mannitol: for ECF (too large to cross membranes)
  • Evans blue: for plasma (binds to serum albumin)
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41
Q

Proximal tubule

A 
EARLY
Reabsorbs:
-Na+
-H2O (TF/PNa+=1.0)
-HCO3-
-glucose
-amino acids
-phosphate
-lactate

Secretes:
-H+

LATE
Reabsorbs:
-Na+ with Cl-

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42
Q

Water clearance = 0

A

During treatment with loop diuretics:
Inhibits NaCl reabsorption in the thick ascending limb—>
-inhibits dilution in the thick ascending limb
-inhibits production of the corticopapillary osmotic gradient

—>
URINE CANNOT BE DILUTED OR CONCENTRATED

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43
Q

Glomerulotubular balance

A

In the proximal tubule maintains constant fractional reabsorption (=67%) of the filtered Na+ and H2O ασχετα απο GFR
thanks to Starling forces, πc in the peritubular capillary blood

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44
Q

Thick ascending limb of the loop of Henle-Potential

A

Lumen-positive potential difference:

Although the Na+-K+-2Cl- cotransporter appears to be electroneutral, some K+ diffuses back into the lumen

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45
Q

Loop diuretics

A

Furosemide, ethacrynic acid, bumetanide

Inhibit the Na+-K+-2Cl- cotransporter at the thick ascending limb of the loop of Henle

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46
Q

Thiazide diuretics

A

Inhibit the Na+-Cl- cotransporter at the early distal tubule

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47
Q

How much of the overall Na+ reabsorption is affected by aldosterone?

A

About 2%

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48
Q

K+ -sparing diuretics

A

Spironolactone (antagonist of aldosterone)
Triamterene, amiloride (act directly on the principal cells)
Decrease K+ secretion in principal cells at the late distal tubule and collecting duct

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49
Q

Acetazolamide

A

Diuretic - Carbonic anhydrase inhibitor

In the early distal tubule by inhibiting the reabsorption of filtered HCO3-

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50
Q

K+ excretion

A

Can vary widely from 1% to 110%

Depending on dietary K+ intake, aldosterone levels and acid-base status (and flow rate)

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51
Q

K+ excretion

A

Can vary widely from 1% to 110%
Depending on dietary K+ intake, aldosterone levels and acid-base status and flow rate (e.g. thiazide increase flow rate at the site of distal tubular secretion –> K+ excretion is increased)

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52
Q

Causes of shift of K+ out of cells —> Hyperkalemia

A 
Insulin deficiency
β-adrenergic antagonists 
Acidosis
Hyperosmolarity
Inhibitors of Na+-K+ pump (digitalis)
Exercise
Cell lysis
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53
Q

Causes of shift of K+ into cells —> Hypokalemia

A

Insulin
β-adrenergic agonists
Alkalosis
Hyposmolarity

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54
Q

Increase of RBF

A 
Caused by
Vasodilation of renal arterioles
produced by
-prostaglandins E2 and I2
-bradykinin
-nitric oxide
-dopamine

Vasodilation of afferent and,to a lesser extent, vasoconstriction of efferent arterioles
Produced by
Atrial natriuretic peptide (ANP)

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55
Q

Buffers

A

Extracellular:

  • HCO3- (CO2/HCO3- pK=6.1)
  • Phosphate (H2PO4-/HPO4-2 pK=6.8) –> URINARY BUFFER

Intracellular

  • Organic phosphates (AMP,ADP,ATP, 2,3-DPG)
  • Proteins: imidazole, α-amino groups, Hemoglobin (deoxy)
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56
Q

Concentration of inulin in the tubular fluid reflects

A

The amount of water remaining in the tubule because inulin once filtered us neither reabsorbed nor secreted

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57
Q

Hypermagnesia

A

Hypocalcemia <—- increased Ca2+ clearance

Because Mg2+ competes with Ca2+ for reabsorption in the thick ascending limb

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58
Q

How alkalosis affects K+

A

Reduced [H+] in blood will cause intracellular H+ to leave cells in exchange for extracellular K+

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59
Q

Filtration fraction=

A

The fraction of RPF filtered across the glomerular capillaries
= GFR/RPF
normally about 0.20
Increases—>^protein concentration of peritubular capillary blood—> ^reabsorption in the proximal tubule
Decreases—> decreased protein concentration of peritubular capillary blood —> decreased reabsorption in the proximal tubule
D

60
Q

How oxygen deprivation affects reabsorption in the proximal tubule?

A

Would inhibit reabsorption by stopping the Na+-K+ pump in the basolateral membranes

61
Q

RBF=

A

RPF/1-Hct= Cpah/1-Hct = (Upah x V/Ppah)/1-Hct

62
Q

Regulation of gastrin secretion

A

Stimuli for secretion:
-small peptides and amino acids
most potent phenylalanine and tryptophan
-distention of the stomach
-vagal stimulation mediated by gastrin-releasing peptide (GRP) NOT ACh!!! (not blocked by atropine)

Inhibition of gastrin secretion:

  • H+ in the lumen of the stomach (negative feedback)
  • Somatostatin
63
Q

HCO3- reabsorption in metabolic alkalosis

A

Normally increased excretion of HCO3- because the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it

BUT
If metabolic alkalosis is accompanied by volume contraction (e.g. vomiting) the reabsorption of HCO3- increases (contraction alkalosis)

64
Q

Striated muscle in the GI tract

A

Pharynx, upper one-third of the espphagus and external anal sphincter

65
Q

Respiratory alkalosis-muscle symptoms

A

Tingling, numbness, muscle spasm=
HYPOCALCEMIA
H+ and Ca2+ compete for binding sites on plasma proteins
Decreased [H+] –> ^ protein binding of Ca2+ and decreased free ionized Ca2+

66
Q

Salicylate intoxication

A

-METABOLIC ACIDOSIS
salicylate acid , ^anion gap

-RESPIRATORY ALKALOSIS
Direct stimulation of medullary respiratory center

67
Q

Parasympathetic innervation of the GI tract (parts)

A

Vagus: esophagus,stomach,pancreas,upper large intestine

Pelvic: lower large intestine,rectum,anus

68
Q

Absorption of vitamins

A

FAT-SOLUBLE (A,D,E,K) :
incorporated into micelles and absorbed along with other lipids

WATER-SOLUBLE:
(most) by Na+ -dependent cotransport mechanisms

VITAMIN B12 :
requires intrinsic factor (secreted by parietal cells)
vitamin B12-intrinsic factor complex binds to a receptor in the ILEAL cells and is absorbed

69
Q

“Official” GI hormones

A

Gastrin
Cholecystokinin (CCK)
Secretin
Glucose-dependent insulinotropic peptide (GIP)

70
Q

Actions of gastrin

A

^ Gastric H+ secretion

Growth of gastric mucosa

71
Q

“Official” GI hormones

A

Gastrin
Cholecystokinin (CCK)
Secretin
Glucose-dependent insulinotropic peptide (GIP)

72
Q

Actions of gastrin

A

^ Gastric H+ secretion

Growth of gastric mucosa

74
Q

Actions of CCK

A

1) contraction of the gallbladder/relaxation of the sphincter of Oddi
2) pancreatic enzyme secretion
3) potentiates secretin-induced stimulation of pancreatic HCO3- secretion
4) growth of the exocrine pancreas
5) inhibits gastric emptying!

75
Q

Actions of secretin

A

1) pancreatic HCO3- secretion + growth of the exocrine pancreas
2) HCO3- and H2O secretion by the liver + bile production
3) INHIBITS H+ secretion by the parietal cells

76
Q

Stimuli for the release of GIP

A

Fatty acids
Amino acids and
ORALLY administered glucose [—> oral glucose is more effective than intravenous glucose in causing insulin release]

77
Q

GLP-1

A

binds to pancreatic β-cells and stimulates insulin secretion [analogues may be helpful in the treatment of type 2 diabetes mellitus]

78
Q

Somatostatin actions

A

inhibits secretion of all GI hormones!!

+ inhibits gastric H+ secretion

79
Q

Neurocrines of the GI tract

A

VIP (vasoactive intestinal peptide)
GRP (bombesin)
Enkephalins

80
Q

Basis for the usefulness of the OPIATES in the treatment of diarrhea

A

Enkephalins inhibit intestinal secretion of fluid and electrolytes

81
Q

Striated muscle in the GI tract

A

Pharynx, upper one-third of the esophagus and external anal sphincter

82
Q

Interstitial cells of Cajal

A

pacemaker of the GI smooth muscle

produce slow waves

83
Q

Slow waves (mechanism)

A

cyclic opening of the Ca2+ channels followed by opening of K+ channels
depol brings the membrane potential closer to threshold —>increases the probability that action potentials will occur

84
Q

How to measure intrathoracic pressure

A

Using a balloon catheter placed in the esophagus

[lower than atmospheric]

85
Q

Relaxation of the Lower Esophageal Sphincter- How

A

Vagally mediated and the neurotransmitter is VIP

86
Q

When is gastric emptying inhibited/slowed?

A

1) when the stomach contents are hypertonic or hypotonic
2) fat (CCK)
3) H+ in the duodenum (direct neural reflexes)

87
Q

Components of the gastrocolic reflex

A
  • rapid parasympathetic component

- slower hormonal component mediated by CCK and gastrin

88
Q

Mechanism of Protein absorption

A

LUMEN –> INTESTINAL CELL:
Na+ - dependent cotransport (amino acids)
H+ - dependent cotransport (di- and tripeptides)

INTESTINAL CELL –> BLOOD
Cytoplasmic peptidases hydrolyze di- and tripeptides to amino acids
All amino acids are transported by facilitated diffusion

89
Q

Pancreatic secretions are …tonic

A

Always isotonic, regardless of flow rate

90
Q

Hormones of the anterior lobe if the pituitary

A

1) Growth hormone
2) Prolactin
3) TSH
4) LH
5) FSH
6) ACTH

91
Q

Which hormones are derived from POMC

A

ACTH
MSH (α- and β-)
β-lipotropin
β-endorphin

92
Q

Regulation of ADH secretion

A

Increased by:

  • ^ serum osmolarity
  • volume contraction
  • pain
  • NAUSEA
  • hypoglycemia
  • nicotine, opiates, antineoplastic drugs

Decreased by:

  • decr serum osmolarity
  • ethanol
  • α-agonists
  • ANP
93
Q

How hepatic failure affects thyroid hormones

A

TBG levels decrease –> decrease in total thyroid hormone levels but normal levels of free hormone

94
Q

How pregnancy affects thyroid hormones

A

TBG levels increase –> increase in total thyroid hormone but normal levels of free hormone = clinically EUTHYROID

95
Q

Thyroid hormones effect on Basic Metabolic Rate (BMR)

A

O2 consumption and BMR are increased in all tissues EXCEPT
brain
gonads and
spleen

due to increase of the synthesis of Na+,K+ ATPase

96
Q

How does thyroid hormone have same actions as the sympathetic NS

A

up-regulates β1-adrenergic receptors in the heart

97
Q

How glucocorticoids stimulate gluconeogenesis

A

1) ^ protein catabolism in muscle (and decrease protein synthesis) –> ^ amino acids provided to the liver for gluconeogenesis
2) decrease glucose utilization and insulin sensitivity of adipose tissue
3) ^ lipolysis –> ^ glycerol provided to the liver for gluconeogenesis

98
Q

Anti-inflammatory effects of glucocorticoids (mechanism)

A

1) induce synthesis of LIPOCORTIN = (-) phospholipase A2 —> (-) liberation of arachidonate from membrane phospholipids —> (-) synthesis of prostaglandin and leukotriene
2) (-) production of IL-2 / proliferation of T lymphocytes
3) (-) release of histamine and serotonin from mast cells and platelets

99
Q

Actions of glucocorticoids (in general)

A

1) Stimulation of gluconeogenesis
2) Anti-inflammatory effects
3) Suppression of the immune response
4) Maintenance of vascular responsiveness to catecholamines (up regulation of α1 - vasoconstriction)

100
Q

Actions of mineralocorticoids

A

PRINCIPAL

  • ^ renal Na+ reabsorption
  • ^ renal K+ secretion

α-INTERCALATED
- ^ renal H+ secretion

101
Q

Differences between Secondary adrenocortical insufficiency and Addison disease

A

Addison disease =primary adrenocortical insufficiency
Secondary adrenocortical insufficiency = primary deficiency of ACTH

DIFFERENCES:
In Secondary :
- NOT hyperpigmentation (because no ACTH)
- NOT volume contraction, hyperkalemia or metabolic acidosis (aldosterone levels are normal)

102
Q

Hormone levels in 21β-Hydroxylase deficiency

A

Decrease in
cortisol and
aldosterone
(and gonadal hormones?)

Increase in
ACTH
adrenal androgens
17-hydroxyprogesterone and 
progesterone
103
Q

Hormone levels in 17α-hydroxylase deficiency

A

Decrease in
androgen and
glucocorticoids

Increase in
mineralocorticoid and
ACTH

104
Q

Why hypotension in diabetes mellitus

A

Result of ECF volume contraction.
high blood glucose –> high filtered load of glucose –> exceeds reabsorptive capacity (Tm) of the kidney –> unreabsorbed glucose acts as an osmotic diuretic

105
Q

When does ovulation occur

A

14 days before menses REGARDLESS of cycle length

106
Q

Basal body temperature during luteal phase

A

Increases because of the effect of progesterone on the hypothalamic thermoregulatory center

107
Q

Major placental estrogen (second and third semester)

A

Estriol

108
Q

Human Placental Lactogen

A

produced throughout pregnancy

actions similar to growth hormone and prolactin

109
Q

Amine hormones

A

Thyroid, epinephrine , norepinephrine

= derivatives of tyrosine

110
Q

Regulation of growth hormone secretion

A

Increased by
Sleep, stress, hormones related to puberty, starvation, exercise, hypoglycemia

Decreased by
Somatostatin, somatomedins, obesity, hyperglycemia, pregnancy

111
Q

Prolactin excess

A

Results from:

  • hypothalamic destruction
  • prolactinoma

Causes:

  • galactorrhea
  • decreased libido
  • failure to ovulate and amenorrhea

Treated with:
bromocriptine

112
Q

Actions of ADH

A

1) ^ H2O permeability (aquaporin 2) on the principal cells of late distal tubule and collecting ducts (V2 receptor)
2) constriction of vascular smooth muscle cell (V1 receptor)

113
Q

Why give oxytocin

A
  • to induce labor

- to reduce postpartum bleeding

114
Q

Iodide pump/Na+ - I- contrasporter is inhibited by

A

thiocyanate and perchlorate anions

115
Q

Peroxidase in the follicular cell membrane is inhibited by

A

Propylthiouracil

—>used therapeutically to reduce thyroid hormone synthesis for the treatment of hyperthyroidism

116
Q

Wolff-Chaikoff effect

A

High levels of I- inhibit organification —> inhibit synthesis of thyroid hormone

117
Q

T3/T4 is more biologically active?

A

T3

118
Q

Hormones that regulate prolactin secretion

A

Dopamine inhibits

TRH increases

119
Q

Actions of ACTH

A
  • Stimulates cholesterol desmolase –> (+) conversion of cholesterol to pregnenolone
  • Up-regulates its own receptor at the adrenal cortex
  • When chronically increased –> hypertrophy of the adrenal cortex
120
Q

Actions of dexamethasone

A

Inhibits ACTH secretion (dexamethasone suppression test)

121
Q

Dexamethasone suppression test

A

High or low dose and

measure CORTISOL levels

122
Q

Regulation of aldosterone secretion

A 
-tonic control by ACTH 
BUT
-separately regulated by the renin-angiotensin system
and
-serum K+
123
Q

Negative Ca2+ balance

A

=Intestinal Ca2+ absorption

124
Q

Positive Ca2+ balance

A

Intestinal Ca2+ absorption > Ca2+ excretion
In growing children
The excess is deposited in the growing bones

125
Q

How serum [Mg2+] affects PTH secretion

A
  • Mild decreases in serum [Mg2+] stimulate PTH secretion

- Severe decreases in serum [Mg2+] inhibit PTH secretion —> symptoms of hypoparathyroidism (hypocalcemia)

126
Q

How is resorption of the organic matrix of bone reflected

A

Increased hydroxyproline excretion

127
Q

Urinary Ca2+ excretion in primary hyperparathyroidism

A

INCREASED because of the increased filtered load (exceeds Tm)

128
Q

Chronic renal failure - Ca2+

A

1) decreased production of 1,25-dihydroxycholecalciferol contributes to decreased ionized [Ca2+]
2) decreased GFR –> decreased filtration of phosphate –> phosphate retention –> ^ serum [phosphate] –> complexes Ca2+ –> decreased ionized [Ca2+]

–> SECONDARY HYPERPARATHYROIDISM

129
Q

Familial hypocalciuric hypercalcemia

A

Inactivating mutations of the Ca2+ -sensing receptors that regulate PTH secretion
Autosomal dominant
Decreased urinary Ca2+ excretion and ^serum Ca2+

130
Q

Variation of FSH and LH levels over the life span

A

CHILDHOOD: hormone levels are lowest , FSH>LH
PUBERTY AND REPRODUCTIVE YEARS: hormone levels increase , LH>FSH
SENESCENCE: hormone levels are highest , FSH>LH

131
Q

Levels of HCG during pregnancy

A

Peak levels at gestational week 9 and then decline

132
Q

Estrogen production during the second and third semester

A

FETAL ADRENAL GLAND: dehydroepiandrosterone-sulfate (DHEA-S) –> hydroxylated in the FETAL LIVER –>PLACENTA: enzymes remove sulfate and aromatize to estrogens

[major placental estrogen: estriol]

133
Q

Factors that decrease the duration of REM sleep

A

Benzodiazepines

Increasing age

134
Q

At which phase of the cardiac cycle(+ECG) is the aortic pressure lowest

A

Just before the ventricle eject (between isovolumetric contraction and rapid ventricular ejection) -
After the QRS

135
Q

Factors that may destroy the BBB

A

Inflammation
Irradiation
Tumors

136
Q

Oxygen-hemoglobin dissociation curve in co poisoning

A

Shift to the left BUT also decrease in total O2-binding capacity —>decreased maximum percent saturation (max= 50%)

137
Q

Where is estradiol synthesized

A

Testosterone is synthesized in ovarian theca cells and diffuses to ovarian granulosa cells where it is converted to estradiol by aromatase. FSH stimulates aromatase

138
Q

How hypercalcemia affects the action of ADH

A

With severe hypercalcemia, Ca2+ accumulates in the inner medulla and papilla of the kidney

139
Q

Diuretics and Ca2+

A

LOOP:
Ca2+ reabsorption is linked to Na+ reabsorption in the loop of Henle –> inhibiting Na+ with a loop diuretic also inhibits Ca2+ reabsoption—> loop diuretics increase Ca2+ excretion
—> treatment of hypercalcemia (volume to be replaced)

THIAZIDE:
increase Ca2+ reabsporption in the early distal tubule –>
decrease Ca2+ excretion
—> treatment of idiopathic hypercalciuria

140
Q

How ^ intracellular Ca2+ excitates smooth muscle cell

A

binds to calmodulin

141
Q

Difference between action potential of a ventricular muscle cell and an atrial muscle cell

A

atrial muscle cells have a much shorter plateau phase and a much shorter overall duration

142
Q

Causes of nephrogenic diabetes insipidus

A
  • Lithium intoxication: inhibits the Gs protein in collecting duct cells
  • Hypercalcemia: inhibits adenylate cyclase
143
Q

Diuretics and Ca2+

A

LOOP:
Ca2+ reabsorption is linked to Na+ reabsorption in the loop of Henle –> inhibiting Na+ with a loop diuretic also inhibits Ca2+ reabsoption—> loop diuretics increase Ca2+ excretion
—> treatment of hypercalcemia (volume to be replaced)

THIAZIDE:
increase Ca2+ reabsporption in the early distal tubule so that urinary Na+ excretion is increased –>
decrease Ca2+ excretion
—> treatment of idiopathic hypercalciuria

144
Q

COPD causes ….ventilation

A

hypoventilation

145
Q

K+ in vomiting

A

Hypokalemia because

  • loss of gastric K+
  • ^aldosterone due to volume contraction
146
Q

No p waves and bizarre QRS complexes

Where did they originate

A

NOT SA node (no p)
NOT AV node (bizarre and not normal QRS)
NOT VENTRICULAR MUSCLE (no pacemaker activity)
!His-Purkinje system yes (pacemaker activity but not normal QRS)

147
Q

Metabolic acidosis + decreased urinary excretion of NH4+ =

A

Chromic renal failure

148
Q

Which GI hormones are secreted by cell of the duodenum

A

Secretin and CCK

Physiology Brs (1 decks)

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