ITE CA2 Endocrine/Metab/Renal/Electrolytes Flashcards
1
Q
Effect of corticosteroids on: WBC, hemoglobin, blood glucose, K, Na, acid/base status, urinary uric acid, urinary calcium.
A
Corticosteroids are associated with leukocytosis, increased hemoglobin, hyperglycemia, hypokalemia, mild hypernatremia, alkalosis, increased urinary uric acid, and increased urinary calcium.
2
Q
FENA cutoff for pre-renal
A
Fractional excretion of sodium is a useful tool in helping to distinguish the cause of acute kidney injury. In general, a FENA < 1% indicates a prerenal cause such as hypovolemia. Greater than 1% points toward ATN or another intrinsic cause.
3
Q
prerenal urine osmolality
A
greater than 500
4
Q
prerenal urine sodium
A
less than 10
5
Q
BUN:Cr ratio
A
prerenal greater than 20
intrinsic/ATN less than 15
postrenal greater than 15
6
Q
FENa cutoffs
A
prerenal <1
intrinsic >2
postrenal >2
7
Q
random urine sodium cutoffs
A
prerenal <20
intrinsic >20
postrenal >40
8
Q
Hypothermia, AMS, non-pitting edema
A
Myxedema coma is an extreme form of hypothyroidism that is classically characterized by altered mental status, hypothermia, and non-pitting edema. It is most commonly seen in patients with chronic hypothyroidism in the setting of a physiologic stressor such as infection and is considered a life threatening emergency.
TrueLearn Insight : Myxedema coma is rare, and most commonly presents to anesthesiologists in the postoperative period after a trigger such as infection, exposure to cold temperatures, and excessive sedation and analgesic medications.
9
Q
Table 3: Summary of PTH, Calcium, and Phosphorus Disorders
DISORDER - INTACT PTH - CALCIUM - PHOSPHORUS
pHPTH
FHH
2? HPTH
Malignancy
Hypo-PTH
(pHPTH = primary hyperparathyroidism, FHH = familial hypocalciuric hypercalcemia, 2? HPTH = secondary hyperparathyroidism, Hypo-PTH = hypoparathyroidism, PTH = parathyroid hormone)
A
Table 3: Summary of PTH, Calcium, and Phosphorus Disorders
DISORDER INTACT PTH CALCIUM PHOSPHORUS
pHPTH increased increased decreased
FHH normal-mild increase increased normal-mild decrease
2? HPTH increased decreased varies
Malignancy decreased increased normal
Hypo-PTH decreased decreased increased
(pHPTH = primary hyperparathyroidism, FHH = familial hypocalciuric hypercalcemia, 2? HPTH = secondary hyperparathyroidism, Hypo-PTH = hypoparathyroidism, PTH = parathyroid hormone)
10
Q
Carcinoid syndrome causes the classic triad of______. Diagnostic testing includes measuring _____
A
Carcinoid syndrome causes the classic triad of flushing, asthma, and right-sided heart disease. Diagnostic testing includes measuring urine 5-hydroxyindoleacetic acid
Lung metabolism of serotonin evidently prevents involvement of the left side of the heart with carcinoid syndrome.
11
Q
Best test to eval hepatic sythesis
A
Prothrombin time (PT) is the most useful to diagnose hepatic synthesis abnormalities because many of the procoagulants in this test are synthesized in the liver. They also have shorter half-lives thus alterations in synthesis are observed faster than with other tests, such as albumin.
12
Q
Factors not produced in the liver
A
III, IV, VIII
13
Q
Where is factor VIII produced
A
endothelial cells and bone marrow
14
Q
Growth hormone
A
Growth hormone is an anabolic hormone; most of its effects are mediated by IGF-1. It causes hyperglycemia and insulin resistance, as seen in patients with acromegaly.
15
Q
where is angiotensin I converted to II
A
pulmonary circulation by ACE
16
Q
Where is renin produced
A
juxtaglomerular apparatus in kidney
17
Q
what does renin do
A
cleaves angiotensinogen into angiotensin I
18
Q
Norepinephrine site of degradation and inactivation
A
pulmonary endothelium and nerve terminals
19
Q
Acromegaly lung volumes
A
Patients with excess growth hormone (GH) actually have increased lung volumes, which causes subsequent ventilation-to-perfusion mismatching.
Resultant manifestations of a GH-secreting pituitary tumor include mass effect side effects (headache, visual field defects, rhinorrhea) and excess growth hormone side effects (skeletal overgrowth such as prognathism, soft-tissue overgrowth, connective tissue overgrowth causing possible recurrent laryngeal nerve paralysis and/or hoarseness, peripheral neuropathy (e.g. carpal tunnel syndrome,), visceromegaly, glucose intolerance, osteoarthritis, osteoporosis, hyperhidrosis, skeletal muscle weakness, increased lung volumes).
20
Q
Lab findings in SIADH
A
1) Urine osmolality >100 mOsm, and often > 200-300 mOsm
2) Fractional excretion of sodium (FENa) > 1%
3) Urine Na+ > 20 mEq/L
4) Low serum uric acid and BUN
5) Dilutional, euvolemic hyponatremia (serum Na+ < 135 mEq/L)
21
Q
what do glucocorticoids do
A
Glucocorticoids act to produce more aldosterone and inhibit the phospholipase A2 enzyme (PLA2). The PLA2 enzyme converts phosphatidylcholine to arachidonic acid, a precursor to prostaglandins, leukotrienes, and other proinflammatory mediators (e.g. TNF-α, interleukin-1, interleukin-6, cellular adhesion molecules).
22
Q
Symptoms of Cushing syndrome
A
Cushing syndrome is characterized by a group of signs and symptoms resulting from prolonged exposure to excess cortisol. Classic symptoms include moon facies, buffalo hump, abdominal weight gain, thinning of the extremities, hirsutism, elevated blood sugar, and mood changes.
Protein synthesis and breakdown become mismatched and the resulting progressive protein loss causes drastic perturbations of body mass composition.
Classic physical signs of EXCESS protein breakdown that characterize Cushing syndrome are increased fatty deposits in the face (moon facies), shoulders, and neck (buffalo hump), truncal obesity, and muscle wasting (thinning) of the upper and lower extremities.
23
Q
anesthetic considerations for Cushing
A
Anesthetic management of patients with Cushing Syndrome focuses on blood pressure regulation (these patients are typically hypertensive), glucose control, balancing electrolytes (often hypokalemia), and positioning (due to osteopenia).
24
Q
Primary hyperthyroidism is characterized by
A
Primary hyperthyroidism is characterized by elevated T3, T4 (free and total), and thyroid hormone binding ratio, and a low or normal TSH
25
Primary hyperthyroidism vs Secondary hyperthyroidism
Primary hyperthyroidism is the term used when the pathology is within the thyroid gland. Secondary hyperthyroidism is the term used when the thyroid gland is stimulated by excessive thyroid-stimulating hormone (TSH) in the circulation.
26
Aldosterone effect on potassium
Aldosterone and cortisol promote renal potassium secretion leading to losses through the urine. Insulin and thyroid hormones enhance cellular potassium uptake.
27
Cortisol effect on potassium
Aldosterone and cortisol promote renal potassium secretion leading to losses through the urine. Insulin and thyroid hormones enhance cellular potassium uptake.
28
Insulin effect on potassium
Aldosterone and cortisol promote renal potassium secretion leading to losses through the urine. Insulin and thyroid hormones enhance cellular potassium uptake.
29
Thyroid hormones effect on potassium
Aldosterone and cortisol promote renal potassium secretion leading to losses through the urine. Insulin and thyroid hormones enhance cellular potassium uptake.
30
indications for emergent dialysis
AEIOU: Acidosis (uncompensated metabolic acidosis with pH below 7.1), Electrolytes, Ingestions (toxins), Overload, Uremia.
31
Perioperative hyperglycemia has been associated with
```
Perioperative hyperglycemia has been associated with
immunosuppression,
increased infections,
osmotic diuresis,
delayed wound healing,
delayed gastric emptying,
sympatho-adrenergic stimulation, and
increased mortality.
```
In addition, it reduces skin graft success, exacerbates brain, spinal cord, and renal damage by ischemia, worsens neurologic outcomes in traumatic head injuries, and is associated with postoperative cognitive dysfunction following CABG.
32
pre-op pheo meds
Preoperatively, patients are commonly treated with phenoxybenzamine, which is a long-acting non-selective α-blocker. Selective α1-blockers, such as doxazosin, terazosin, and prazosin, are also commonly used.
33
Angiotensin II causes ___
```
Angiotensin II results in
increased inotropy,
chronotropy,
catecholamine release,
catecholamine sensitivity,
aldosterone levels,
vasopressin levels, and
cardiac remodeling through AT1 receptors.
```
ACE inhibitors and ARBs help to prevent the remodeling that occurs secondary to angiotensin II and are beneficial in congestive heart failure.
34
substances commonly removed from patient's blood in dialysis
Substances that are commonly removed from the patient’s blood include calcium, creatinine, magnesium, phosphate, potassium, urea, and free water.
35
substances may be added or removed from blood by dialysis
Substances that may be added to, or removed from, the patient’s blood include bicarbonate, chloride, glucose, and sodium.
36
dialysis effect on albumin or prealbumin
Serum concentrations of larger molecules such as proteins are usually (transiently) increased following HD due to a concentrating effect from the removal of free water. The absolute amount of these substances in blood stays approximately the same.
37
Metabolic Changes Associated With TPN:
Metabolic Changes Associated With TPN:
- Hypophosphatemia
- Hyperglycemia
- Hypercarbia
- Hypokalemia
- Hypomagnesemia
- Hyperinsulinemia
38
respiratory quotient
respiratory quotient of 0.7 would be pure lipid oxidation and a quotient of 1.0 would be pure carbohydrate oxidation.
39
Acute respiratory acidosis compensation
An acute respiratory acidosis is compensated with an increase in HCO3- of 0.2 mmol/L for each 1 mm Hg increase in PaCO2 above 40 mm Hg
40
Chronic respiratory acidosis compensation
A chronic respiratory acidosis is compensated with an increase in HCO3- of 0.4 mmol/L for each 1 mm Hg increase in PaCO2 above 40 mm Hg.
41
Type 1 hepatorenal syndrome
Type I HRS is an acute and rapid renal failure (doubling of serum creatinine) associated with a precipitating cause (e.g. spontaneous bacterial peritonitis, sepsis, surgery), that responds to medical therapy and stabilizes even after medical therapy is discontinued. Without treatment, the median survival is 2-4 weeks for type I HRS.
42
Type 2 hepatorenal syndrome
Type II HRS is an insidious onset of renal failure as a result of portal hypertension. Loss of intravascular volume from splanchnic dilation and ascites formation is compensated for with increased renal vasoconstriction and activation of the sympathetic, renin-angiotensin, and vasopressin systems
43
Propylthiouracil (PTU) and methimazole (MTZ)
Propylthiouracil (PTU) and methimazole (MTZ) are both medications that can be used to inhibit the production of thyroid hormone (T4).
In addition, propylthiouracil blocks the peripheral conversion of T4 to T3 - this makes PTU favorable over MTZ
44
thyroid storm treatment
Thyroid hormone release can be blocked by sodium or potassium iodide administration, however only after a thyrostatic medication such as propylthiouracil has been given. plus supportive treatment
45
A 56-year-old female is being monitored in the intensive care unit after presenting with a subarachnoid hemorrhage. On post-bleed day 2, the patient is noted to have new onset hyponatremia. On exam the patient appears euvolemic. Further workup reveals a high urine sodium and high urine osmolarity. Which of the following is MOST likely?
SIADH
Hyponatremia with euvolemia or hypervolemia is most likely syndrome of inappropriate antidiuretic hormone secretion (SIADH) in this patient
46
cerebral salt wasting volume status
hypovolemic
47
EKG changes hypocalcemia
shortened PR
prolonged QT*** classic
T wave inversion
48
EKG changes hypokalemia
```
PR prolonged
QRS narrowed
QT prolonged
T waves flat
U waves
```
49
EKG changes hypomagnesemia
PRshortened
QRS narrowed
QT prolonged
50
EKG changes hypercalcemia
PR prolonged
QRS widened
QT shortened
T waves peaked
51
EKG changes hyperkalemia
PR prolonged
QRS widened
T waves peaked
52
EKG changes hypermagnesemia
PR prolonged
| QRS widened
53
Vasopressin secretion stimultated by
| inhibited by
Vasopressin secretion is stimulated by increased plasma osmotic pressure, decreased intravascular volume, and systemic arterial hypotension. Vasopressin secretion is also mediated by certain hormonal triggers: AT2 stimulates vasopressin secretion while ANP inhibits secretion.
54
Oxytocin similar in structure to what
Vasopressin’s structure is similar to oxytocin; their amino acid sequences only differ by two amino acids. As a result, the two peptides exhibit some cross-reactivity at high plasma concentrations: vasopressin can cause uterine contractions while oxytocin can slightly inhibit diuresis.
55
Vasopressin receptors
Activation of V2 receptors in the renal collecting ducts causes water reabsorption and an increase in circulating volume.
Activation of smooth muscle V1 receptors in blood vessels causes vasoconstriction (especially in splanchnic vasculature). This effect is particularly important at the renal efferent glomerular arterioles where it serves to maintain glomerular filtration pressure.
56
other name for somatostatin and what does it do
Somatostatin, also known as growth hormone-inhibiting hormone (GHIH), inhibits insulin secretion. It also inhibits glucagon and thyroid stimulating hormone (TSH).
57
cholecystokinin does what to insulin
increase
58
gastric inhibitory peptide does what to insulin
increase
59
somatostatin does what to insulin
decrease
60
what does glucagon do for blood sugar
- stimulates hepatic glycogenolysis
- stimulates hepatic gluconeogenesis
- stimulates lipolysis
- inhibits hepatic glycolysis
- inhibits hepatic glycogen synthesis
RESULT IS RAISED BLOOD GLUCOSE
61
Other effects of glucagon include, but are not limited to:
Other effects of glucagon include, but are not limited to:
- Decreased gastric motility
- Relaxation of smooth muscle
- Decreases biliary sphincter and lower esophageal sphincter tone
- Mild generalized vasodilation
- Dilates hepatic arterioles and increases hepatic and splanchnic blood volume
- Antagonizes vasoconstrictor effects of catecholamines
- Enhanced urinary excretion of inorganic electrolytes
Glucagon also has cardiac inotropic and chronotropic effects. Similar to catecholamines, it enhances activation of adenyl cyclase in cardiac myocytes, but its effects are NOT blocked by β-blockers. Typical dose is 1-5 mg IV followed by an infusion.
62
Adrenal insufficiency electrolyte disturbances
Adrenal insufficiency is more likely to manifest with hyponatremia, hyperkalemia, hypercalcemia, and hypoglycemia.
63
addisons disease
adrenal insufficiency
64
anabolic stuff insulin does
myocytes: increase glucose uptake, increase amino acid uptake, increase glycogen storage, increase protein synthesis
adipocytes: increase glucose uptake, increase fatty acid storage
hepatocytes: increase macronutrient uptake, increase glycogen synthesis, increase fatty acid synthesis
65
catbolic stuff that insulin inhibits
Insulin also inhibits catabolic processes throughout the body. Within the liver, it inhibits glycogenolysis and gluconeogenesis. Throughout the body, it inhibits lipolysis, protein breakdown (proteolysis), ketone formation, and oxidation of fatty acids and amino acids.
66
causes of anion gap
Causes of an anion gap include the mnemonic GOLDMARK:
- Glycols (ethylene, propylene)
- Oxoproline (acetaminophen toxicity in malnourished/diabetics)
- L lactic acid
- D lactic acid
- Methanol
- Aspirin
- Renal failure
- Ketoacids (diabetes, starvation, alcohol)
67
Causes of a non-gap acidosis
Causes of a non-gap acidosis include administration of normal saline, gastrointestinal losses (diarrhea, high-output ileostomy, fistula), renal losses (renal tubular acidosis), and certain drugs (such as acetazolamide).
68
Lab findings suggestive of ATN include:
```
Lab findings suggestive of ATN include:
muddy brown casts,
FENa > 1%,
Uosm < 350 mOsm/kg,
UNa > 40 mEq ,
low specific gravity, and
BUN:Cr 10:1 – 15:1.
```
69
urine sodium content in ATN
Destruction of the tubular and epithelial cells in ATN impairs the kidney's ability to concentrate the urine and retain sodium. As a result, the urine is typically diluted with a high Na content
70
what carries highest risk for post cardiopulmonary bypass acute kidney injury.
Elevated preoperative creatinine, complex cardiac procedures, emergency surgery, and preoperative intraaortic balloon pump carry the highest risk for post cardiopulmonary bypass acute kidney injury.
Other well-known minor risk factors include: female gender, congestive heart failure, chronic obstructive pulmonary disease, insulin-requiring diabetes, and depressed left ventricular ejection fraction.
71
Renal compensation for respiratory acidosis
Renal compensation for respiratory acidosis occurs at a slow rate. In acute respiratory acidosis, serum bicarbonate levels increase 1 mEq/L for each 10 mm Hg rise in PaCO2. If the respiratory acidosis is chronic, bicarbonate levels increase between 4-5 mEq/L for each 10 mm Hg rise in PaCO2.
72
signs of hypocalcemia
Hypocalcemia is a complication found following a parathyroidectomy. Signs and symptoms include distal paresthesias, tetany, anxiety/psychosis, abdominal cramps, urinary frequency, and in severe cases seizures and laryngospasm. Immediate repletion of calcium is necessary if these signs are present.
73
fluid-induced metabolic acidosis mechanism
But an important point to recognize is that fluid-induced metabolic acidosis can also result from infusions containing low Cl- (0.45% saline or mannitol). The reason for this is because the metabolic acidosis is not due to the chloride, rather due to the reduction in SID. Large infusions of fluid that have a SID of zero will dilute the plasma SID (normal is 40 mEq/L). This results in "dilutional" acidosis.
SID = strong ion difference
74
How does hyperchloremia affect strong ion difference
In the setting of hyperchloremia (from large saline infusion) the plasma Cl- concentration increases which results in a decrease in HCO3- to maintain net neutrality. The decrease in HCO3- reduces the SID.
75
strong ion difference and pH
As SID decreases, pH decreases, and vice versa.
76
SID takes into account what ions
SID takes into account HCO3-, albumin, phosphate, and unmeasured anions.
77
normal strong ion difference
40
78
FENa = formula
```
FENa = Excreted Na/Filtered Na x 100 = (UNa x PCr)/(UCr x PNa x 100)
UNa – urine sodium
PNa – plasma sodium
UCr – urine creatinine
PCr – plasma creatinine
```
79
adrenal cortex does what in response to what
| adrenal medulla does what in response to what
The adrenal gland consists of two grossly and functionally distinct zones. The outer cortex secretes steroid hormones in response to fluid/electrolyte shifts and ACTH. The adrenal medulla secretes catecholamines in response to direct innervation by preganglionic sympathetic fibers.
80
primary adrenal insufficiency is a result of what
Primary adrenal insufficiency is a result of intrinsic adrenal gland dysfunction.
81
secondary adrenal insufficiency is a result of what
| what electrolyte derrangements
Secondary adrenal insufficiency is a result of decreased ACTH, which is most commonly due to exogenous steroid administration.
Generally, mineralocorticoid production remains adequate in secondary adrenal insufficiency, so fluid/electrolyte derangements are often not seen.
Therefore, treatment with an exogenous glucocorticoid (e.g. dexamethasone) would be appropriate. (methylprednisolone is not needed)
82
Metabolic alkalosis can be caused by
Metabolic alkalosis can be caused by blood product administration; gastric losses, urinary loses, or excessive exogenous bicarbonate administration.
83
alkalosis and calcium
Hypocarbia resulting from the patient hyperventilating during venipuncture could result in respiratory alkalosis. This alkalosis could, in turn, result in a decrease in the ionized fraction of calcium in the serum, causing functional hypocalcemia. Symptoms of this hypocalcemia would include perioral numbness along with tingling in the hands and feet.
The second effect stems from the alkalinization of the serum itself. This results in a decrease in the fraction of calcium that is ionized due to increased binding of calcium to albumin. As ionized calcium is the functional form of calcium in the serum, this results in functional hypocalcemia. Symptoms such as tingling in the hands and feet, cramping, and eventually tetany can occur following hyperventilation.
84
The renal medulla extracts oxygen at a ratio of
The renal medulla extracts oxygen at a ratio of ~80% making it exquisitely sensitive to small changes in renal blood flow. The mechanisms of many perioperative renal insults are based on the disruption of adequate blood flow (and therefore oxygen delivery) to the renal medulla.
85
blood flow in and oxygen extraction in the kidneys
The kidneys receive approximately 20% of the cardiac output. Whereas in many organs, the oxygen extraction ratio is ~45%, it is much lower in the kidneys when considered as a whole, at < 20%. A critical difference, however, is the contrast between the renal cortex and the medulla.
The renal cortex receives the lion’s share of the blood flow (~94%) but exhibits an oxygen extraction ratio of 18-20%. This leads to a relatively high PO2 within the renal cortex. The medulla, on the other hand, receives the remaining 6% of the renal blood flow but has an oxygen extraction ratio of nearly 80%. Because of this, a small change in total blood flow to the kidney could have exaggerated effects in the medulla causing local hypoxia and subsequent injury.
86
how do NSAIDs damage kidneys
In this region, prostaglandins cause vasodilation, increasing blood flow. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the synthesis of these compounds, preventing the increase of blood flow to the medulla
87
what does angiotensin II do
Angiotensin II causes efferent glomerular arteriolar vasoconstriction which will maintain or increase glomerular filtration rate (GFR) in states of hypovolemia.
Angiotensin II then promotes aldosterone production. Angiotensin II and aldosterone both act to increase intravascular volume, raise systemic blood pressure, and maintain adequate GFR.
Angiotensin II also promotes release of antidiuretic hormone (ADH) which increases renal collecting duct water absorption and SVR.
88
Hyperparathyroidism can cause what electrolyte abnormalities
| and acid/base status
Hyperparathyroidism can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis.
89
what does juxtaglomerular apparatus sense
| what results if it senses decreased renal blood flow
When renal blood flow (RBF) decreases from a variety of factors, the concurrent decrease in glomerular filtration rate (GFR) leads to a decrease in the amount of chloride that is sensed at the juxtaglomerular (JG) apparatus. When there is decreased chloride concentration at the JG apparatus, the afferent arterioles dilate and increase glomerular flow and GFR. In addition, the decreased chloride concentration leads to the release of renin from the JG apparatus, ultimately causing vasoconstriction of the efferent arterioles by angiotensin II.
90
Where does T3 come from
The thyroid secretes T3 and T4, which are the regulators of metabolism and homeostasis. Most T3, the more potent hormone of the two, is formed through peripheral conversion of T4.
91
what drug decreases T4 to T3 conversion
The process of peripheral T4-to-T3 conversion is targeted in treating hyperthyroidism with the drug propylthiouracil (PTU). In addition to central thyroid inhibition by inhibiting thyroperoxidase, PTU decreases peripheral conversion by inhibiting 5'-deiodinase.
92
what is the neurohypophysis
posterior pituitary gland
| secretes oxytocin, vasopressin
93
Sodium bicarbonate amount that will normalize blood pH
Sodium bicarbonate can be administered perioperatively to correct a metabolic acidosis. The amount that will normalize blood pH can be approximated with the formula:Sodium bicarbonate (mEq) = 0.2 * patient weight (kg) * base deficit.
94
Treatment for hyperkalemia includes
Treatment for hyperkalemia includes, but is not limited to, albuterol, insulin, sodium bicarbonate, sodium polystyrene sulfonate, loop diuretics, and/or hemodialysis. Albuterol and insulin are rapid acting and the most effective pharmacologic interventions for acutely lowering serum potassium. Calcium does not affect potassium levels.
Calcium chloride and calcium gluconate stabilize cardiac myocyte membranes. Though onset is immediate, it has no effect on serum potassium levels and thus is not used to lower potassium levels.
95
what does angiotensin II do
Angiotensin II acts on the zona glomerulosa of the adrenal cortex to release the mineralocorticoid, aldosterone. Angiotensin II also acts on other systems – in the blood vessels it stimulates smooth muscle contraction, in the brain, it activates thirst centers, and in the posterior pituitary it stimulates the release of antidiuretic hormone. Angiotensin II and aldosterone both act to maintain fluid balance and blood pressure.
96
Conn syndrome
Conn syndrome is mineralocorticoid excess. It results in potassium depletion, sodium retention, polyuria, tetany, and weakness.
97
what does adrenal medulla produce
| what amino acid does it start with
The adrenal medulla is an endocrine gland that produces dopamine, epinephrine, and norepinephrine. The initial step in catecholamine synthesis is the production of DOPA from the amino acid tyrosine.
98
main function of principal cells in collecting tubule
ADH-mediated sodium reabsorption
99
does nicardipine decrease likelihood of cardiac remodeling
no
100
renal failure cause acidosis or alkalosis
acidosis
101
what structure is responsible for the release of renin
macula densa
102
what portion of the nephron is impermeable to water
distal convoluted tubule
103
U wave on EKG
hypokalemia
104
chlorthalidone affect on calcium
hypercalcemia
105
portion of nephron responsible for majority of sodium reabsorption
proximal convoluted tubule
106
where does cortisol act
Glucocorticoids diffuse through cell membranes to bind to specific receptors that then alter gene transcription.
107
what does cortisol do
Cortisol acts with epinephrine and glucagon to enhance transcription of genes responsible for producing gluconeogenic enzymes such as glucose-6-phosphate.
The end product is the mobilization of fatty acids, catabolism, and an increase in blood glucose levels.
This occurs through the stimulation of gluconeogenesis. Additionally, sensitization of adipose tissue to the action of lipolytic hormones and increased proteolysis by blockage of antiproteolytic actions of insulin act to increase energy substrates. Cortisol causes an increase in insulin resistance decreasing the glucose uptake system.
108
signs/symptoms of hypercalcemia
Hypercalcemia leads to "stones, bones, abdominal groans, thrones, and psychiatric overtones"
Stones: kidney stones
Bones: bone-related complications
Groans: gastrointestinal symptoms
Thrones: polyuria, constipation (throne = toilet)
Overtones: central nervous system effects
Hyperparathyroidism is most often manifested by hypercalcemia, which can lead to preoperative skeletal weakness and unpredictable response to neuromuscular blocking agents.
Hypercalcemia can result in a range of other signs and symptoms. These include nephrolithiasis, polyuria, polydipsia, decreased GFR, anemia, shortening of the QT interval, prolongation of the PR interval, systemic hypertension, abdominal pain, emesis, peptic ulcers, pancreatitis, skeletal demineralization, pathologic fractures, psychosis, decreased pain sensation, and somnolence.
109
signs/symptoms hypophosphatemia
Hypophosphatemia is another manifestation of hyperparathyroidism. It can result in impaired cardiac contractility, congestive heart failure, skeletal muscle weakness, hemolysis, and platelet dysfunction.
110
Angiotensin-II-mediated vasoconstriction is produced within ___nminutes after the onset of acute hypotension or hypovolemia.
Angiotensin-II-mediated vasoconstriction is produced within 20 minutes after the onset of acute hypotension or hypovolemia. The release of A2 is modulated by the RAAS. Blockade of the RAAS by ACEIs and ARBs may cause profound and refractory perioperative hypotension, particularly after induction of general anesthesia.
111
What is cholecystokinin
a hormone which is secreted by cells in the duodenum and stimulates the release of bile into the intestine and the secretion of enzymes by the pancreas.
112
steroid myopathy symptoms and electrolyte changes
Chronic or high-dose use of steroids can lead to myopathy. It often presents with proximal muscle weakness and normal levels of creatine kinase.
113
A mnemonic to help remember the signs and symptoms of hyperthyroidism
A mnemonic to help remember the signs and symptoms of hyperthyroidism is "THYROIDISM" for Tremor, Heart rate up, Yawning (fatigue), Restlessness, Oligomenorrhea & amenorrhea, Intolerance to heat, Diarrhea, Irritability, Sweating, Muscle wasting & weight loss, Exophthalmos.
114
Acute respiratory acidosis is compensated by
| Chronic respiratory acidosis is compensated by
Acute respiratory acidosis is compensated by an increase in serum HCO3- of 2 mmol/L for every 10 mm Hg increase in PaCO2.
Chronic respiratory acidosis is compensated by an increase in serum HCO3- of 4 mmol/L for every 10 mm Hg increase in PaCO2.
115
acetazolamide acid/base
hyperchloremic metabolic acidosis
116
furosemide acid/base disturbance
hypokalemic-hypochloremic metabolic alkalosis
117
what diuretics cause alkalosis
thiazides and loops
118
what diuretics cause acidosis
acetazolamide and potassium-sparing
119
thiazide diuretics acid/base disturbance
hypokalemic-hypochloremic metabolic alkalosis
120
k-sparing diuretics acid/base
hyperchloremic metabolic acidosis
121
cAMP in general does what
smooth muscle relaxation
