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CCP Semester 2: The Path Of Shame > CCP 229 Endocrine > Flashcards

CCP 229 Endocrine Flashcards

1
Q

initial approach to potassium balance in DKA

A
  1. If K+ is ≥3.3 mmol/L, start insulin infusion
  2. If K+ is <3.3 mmol/L, replenish potassium before initiating insulin infusion

be smart though. like, if the dude’s potassium is 3.4, and you’re pumping in like 4L of fluid, there’s probably gonna be some element of dilutional hypokalemia and you should probably put a couple bags of K+ in before you start the insulin. like this isn’t a hard and fast thing

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2
Q

when is sodium bicarb indicated in DKA?

A
  1. severe hyperkalemia (K+ >6.5 mmol/L)
  2. cardiac arrest
  3. profound shock due to circulatory collapse from acidosis (pH of <6.9)
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3
Q

Diagnostic criteria for DKA

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A
  1. glucose >13 mmol/L
  2. pH ≤7.3
  3. serum bicarbonate ≤16 mmol/L
  4. presence of ketones in serum and urine
  5. anion gap >12 mEq/L
  6. positive betahydroxybutyrate

if the guy is hyperglycaemic, but there’s no beta, it can’t be DKA

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4
Q

patient populations who tend to present with “euglycemic DKA”

A
  1. alcoholics
  2. pregnant patients
  3. diabetics on sodium-glucose cotransporter-2 inhibitors (the “flozin” drugs)
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5
Q

how is the severity of DKA quantified

A
  1. defined as mild, moderate, or severe

2. quantified according to the severity of acidosis (pH, serum bicarbonate, and anion gap)

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6
Q

what patient population is at risk for DKA associated Cerebral edema

A

paediatric patients

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7
Q

the “5 I’s” leading to DKA

A
  1. Infections (most common cause worldwide)
  2. Inadequate insulin (medication noncompliance)
  3. Ischemia or Infarction
  4. Intoxication
  5. Illness
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8
Q

The primary ketone bodies present in DKA

A
  1. acetoacetate

2. beta-hydroxybutyrate

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9
Q

main tenets of DKA management

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A
  1. Airway, breathing, circulation
  2. Commence fluid resuscitation (plasma-lyte or LR)
  3. Treat potassium
  4. Replace insulin (blood glucose should not be corrected by >3 mmol/L per hour)
  5. Acidosis management (bicarb for pH <6.9)
  6. Prevent complications (too fast a reversal of the hyperglycaemia/osmolarity)
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10
Q

why do DKA patients have altered serum K+ levels?

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A
  1. increased levels of ketones in the body leads to extracellular H+
  2. extracellular H+ is exchanged for intracellular K+ in an attempt to improve worsening metabolic acidosis
  3. Patients in DKA experience osmotic diuresis
  4. Extracellular K+ is excreted via the urine, eventually leading to an overall depletion of K+ in both the intravascular and intracellular spaces
  5. Monitor K+ levels closely and replaced as required
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11
Q

why do DKA patients have altered fluid balance?

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A
  1. Hyperglycemia leads to osmotic diuresis due to glucose spilling into the urine from decreased renal reabsorption of glucose
  2. Glucose in the urine leads to increased urinary excretion of water and consequently dehydration
  3. DKA patients can be very dry. Require volumes of up to 6-10L
  4. Half of the fluid resuscitation volume is initially replaced over the first eight hours, with the rest being administered over the next sixteen hours
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12
Q

Why should one be wary of the “serum K+” obtained on initial labs in DKA

A
  1. K+ is regularly lost in DKA
  2. People in DKA have a high propensity to vomit, which decreases K+
  3. Additionally, the osmotic diuresis leads to increased renal excretion of K+
  4. K+ ions buffer H+ ions in acidosis, leading to a higher amount of extracellular K+
  5. Consequently, “total-body potassium” levels are often significantly lower than the initial serum potassium levels would suggest

ie, they don’t actually have that much potassium in their body but because the cells are puking out a shit load of potassium into the serum it APPEARS as though they have a bunch of K+ but really its just gonna get flushed out ASAP so they are net low on K+

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13
Q

pathophysiological pathway of DKA (this one’s a doozy…)

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A
  1. Stress response (5 I’s). Stimulates the adrenal cortex, adrenal medulla, and pituitary glands
  2. Hormonal alterations. Decreased insulin, increased cortisol and glucagon result in increased glycogen to glucose conversion
  3. Gluconeogenesis. The generation of glucose from non-carbohydrate substances within the body.
  4. Gluconeogenesis leads to lipolysis and production of ketone bodies, causing keto acidosis. K+ shifted out of cells to exchange for H+ to reduce systemic acidosis.
  5. Gluconeogenesis causes systemic hyperglycaemia
  6. systemic hyperglycaemia causes glycosuria, causing an osmotic diuresis
  7. polyuria leads to loss of intravascular volume and electrolytes, especially K+
  8. worsening hypovolemia leads to hypotension, shock, coma, death.
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14
Q

criteria for “mild” DKA

A
  1. pH 7.25 – 7.30
  2. bicarbonate 15–18 mmol/L
  3. patient is alert
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15
Q

criteria for “moderate” DKA

A
  1. pH 7.00 – 7.25
  2. bicarbonate 10–15 mmol/L
  3. patient is decreased LOC
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16
Q

criteria for “severe” DKA

A
  1. pH below 7.00
  2. bicarbonate below 10 mmol/L
  3. unresponsive/comatose
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17
Q

define Hyperosmolar hyperglycemic state (HHS)

A

complication of diabetes mellitus in which hyperglycemia results in high osmolarity without significant ketoacidosis

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18
Q

most common trigger for HHS

A

Infection

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19
Q

diagnostic criteria for HHS

A
  1. glucose > 33.3 mmol/L
  2. serum bicarbonate >19 mmol/L
  3. serum osmolality >320 mOsm/kg
  4. absence of ketonemia and ketonuria
  5. Altered sensorium and neurologic findings (hallmarks of the diagnosis)
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20
Q

pathophysiology of HHS

A
  1. In the setting of a physiologic stressor such as infection, serum glucose levels rise precipitously d/t insulin resistance
  2. Because the body has difficulty utilizing glucose d/t insulin resistance, counter-regulatory hormones such as glucagon are released
  3. As a result of glucagon release, the initiation of gluconeogenesis and glycogenolysis occurs and leads to further increases in glucose, causing profound osmotic diuresis and dehydration
  4. The dehydration contributes to prerenal kidney injury
  5. The profound osmotic diuresis significantly increases serum osmolarity, which contributes to altered sensorium
  6. The average fluid deficit in adults in HHS is 9L
  7. Serum K+ levels are falsely elevated because of increased serum concentration from osmotic diuresis and decreased uptake by the cells from insulin insufficiency
  8. Total body K+ is lower because of increased renal losses
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21
Q

treatment pathway for HHS

A

Most of the treatment algorithm for HHS has been extrapolated from DKA management

  1. Airway, breathing, circulation
  2. Commence fluid resuscitation (be careful in fluid administration, because patients are commonly older and more likely to have resultant kidney or cardiac compromise)
  3. Treat potassium
  4. Replace insulin (blood glucose should not be corrected by >3 mmol/L per hour)
  5. Acidosis management (bicarb for pH <6.9)
  6. Prevent complications (too fast a reversal of the hyperglycaemia/osmolarity)
22
Q

define “adrenal insufficiency”

A

the physiologic demand for glucocorticoids (cortisol) and/or mineralocorticoids (aldosterone) exceeds the supply from the adrenal cortex

23
Q

key findings of “adrenal crisis”

A
  1. a patient’s hypotension does not respond to fluid resuscitation and/or vasopressors
  2. classic electrolyte abnormalities of adrenal crisis (hyponatremia, hyperkalemia)
  3. hypoglycemia which does not respond to dextrose
  4. high-risk groups such as patients on long-term steroids or with a known autoimmune disorder, HIV, tuberculosis, or head trauma
24
Q

primary treatment for adrenal crisis

A
  1. Treatment is steroid replacement
  2. Hydrocortisone is first-line treatment because of its glucocorticoid and mineralocorticoid effects
  3. Dexamethasone is an alternative
25
Q

define Pheochromocytoma

A
  1. a catecholamine-secreting tumor of the adrenal medulla

2. may precipitate life-threatening hypertension and multi-organ system failure

26
Q

emergency treatment for Pheochromocytoma

A
  1. Alpha blockade should be given first (phentolamine)
  2. beta blockers
  3. calcium channel blockers
  4. blood pressure control agents as needed for resistant hypertension (Nicardipine, clevidipine, sodium nitroprusside)
27
Q

definitive treatment for Pheochromocytoma

A

Adrenalectomy is the definitive management

28
Q

key findings in adrenal crisis

A
  1. hypotension/shock (90%)
  2. abdominal/flank/back/lower chest pain (86%)
  3. fever (66%)
29
Q

structure and physiology of the adrenal glands

A
  1. The adrenal gland is made up of 2 parts, the cortex and medulla
  2. The medulla produces catecholamines, including epinephrine, norepinephrine, and dopamine
  3. The adrenal cortex produces the mineralocorticoids aldosterone; cortisol; and androgen
30
Q

function and physiologic pathway of cortisol

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A
  1. Cortisol normally facilitates the body’s response to stress (trauma, infection) by influencing the immune system, vascular tone, and metabolism
  2. Cortisol is regulated by the hypothalamic-pituitary-adrenal axis.
  3. In the HPA-axis, the hypothalamus produces corticotropin-releasing hormone, which stimulates the anterior pituitary to produce ACTH
  4. ACTH in turn stimulates the adrenal gland to produce cortisol
31
Q

function and physiologic pathway of aldosterone

A
  1. Aldosterone normally maintains the body’s salt balance and blood pressure
  2. In the setting of decreased blood flow to the kidney (as in hypovolemia), aldosterone causes the renal nephrons to conserve Na+ and to secrete K+ and H+
  3. Aldosterone is regulated by the RAAS
32
Q

define “adrenal crisis”

A
  1. Adrenal crisis is an acute life-threatening presentation of adrenal insufficiency
  2. can be caused by an acute stressor in those with baseline adrenal insufficiency (most common) or by sudden damage to the hypothalamic-pituitary-adrenal axis
  3. In adrenal crisis, the body’s supply of cortisol and/or aldosterone cannot meet the demand for these hormones elicited by the physiologic stressor
33
Q

define “primary adrenal insufficiency”

A
  1. In primary adrenal insufficiency, the immune system or another process directly impacts the adrenal cortex, leading to decreased cortisol, aldosterone, and androgens
34
Q

define “secondary adrenal insufficiency”

A
  1. Secondary adrenal insufficiency is failure of the pituitary gland to produce adequate ACTH
  2. Low ACTH levels result in low levels of endogenous cortisol, leading to symptoms of secondary adrenal insufficiency
  3. most common cause is abrupt withdrawal of prolonged glucocorticoid therapy
35
Q

thyroid storm definition

A
  1. life-threatening condition characterized by severe manifestations of thyrotoxicosis (hyperpyrexia, cardiovascular dysfunction, altered mentation)
36
Q

myxedema coma definition

A
  1. severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs
37
Q

thyroid storm treatment algorithm

A
  1. ABC’s
  2. Beta blockers
  3. Anti-thyroid medications
  4. Iodine
  5. Hydrocortisone
  6. prevent hyperthermia with passive cooling and tylenol
38
Q

pathophysiology of thyroid storm

A
  1. A hyperthyroid state produces excess T4 and T3
  2. Thyroid storm is almost always associated with a trigger, such as sepsis, pregnancy, recent surgery, discontinuation of anti-thyroid medication, etc.
  3. During thyroid storm, the amount of free or unbound thyroid hormone increases
  4. Thyroid storm causes an adrenergic activation leading to increased catecholamine release
  5. The hypermetabolic state causes increased cardiac myocyte production of ATP, which increases the contractility and HR, leading to a high cardiac output
  6. This state also causes increased O2 consumption, which leads to arterial relaxation and decreased SVR.
  7. This activates the RAAS, resulting in an expanded blood volume and leading to an increased preload and a decreased afterload
  8. High output cardiac failure ensues, followed by complete cardiovascular collapse
39
Q

3 basic tenets of treating thyroid storm

A
  1. Block the effects of thyroid hormone
  2. Decrease the levels of circulating thyroid hormone
  3. Treating the inciting event and providing supportive care
40
Q

myxoedema coma treatment algorithm

A
  1. ABC’s
  2. IV thyroid hormone (Levothyroxine)
  3. High dose Hydrocortisone
  4. Vasopressors for shock
  5. Electrolyte replacement
  6. Passive warming
41
Q

pathophysiology of myxoedema coma

A
  1. hypothyroidism is due to a lack of thyroid hormone T3
  2. hypothyroidism progresses to decompensated hypothyroidism after a triggering event (typically infection)
  3. hypothyroidism results in hypothermia and negative cardiac inotropy
  4. The body will attempt to compensate for these alterations with peripheral vasoconstriction
  5. This leads to diastolic HTN and low CO d/t increased afterload
42
Q

most common abnormal vital sign in decompensated hypothyroidism

A
  1. hypothermia d/t hermoregulatory system dysfunction
43
Q

2 basic tenets of treating decompensated hypothyroidism

A
  1. supportive care

2. thyroid hormone replacement therapy

44
Q

how much will 10 mEq of potassium chloride increase serum K+ levels?

A

10 mEq of potassium chloride will roughly increase serum levels by 0.1 mEq/L

45
Q

what is the role of lab data in DKA

A

DKA is diagnosed purely on the basis of venous blood chemistries (chem-7, anion gap, and beta-hydroxybutyrate

  1. diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level)
  2. serum bicarbonate can be used as an index of acidosis severity
  3. pCO2 (which shows how well ventilation is compensating for the metabolic acidosis) may allow detection of patients with inadequate respiratory compensation (occult ventilatory failure), who might benefit from ventilatory support (superimposed respiratory acidosis, might have to tube em’)
46
Q

The case for venous rather than arterial blood gases in diabetic ketoacidosis

A

“In patients with DKA the weighted average difference between arterial and venous pH was 0.02 pH units”

“For bicarbonate, 7 studies with just over 900 patients were reviewed showing a weighted mean difference of -1.41 mmol/L”

“ABG vs VBG analysis changed ED physicians diagnosis in 1%”

Kelly AM. The case for venous rather than arterial blood gases in diabetic ketoacidosis. Emerg Med Australas. 2006

47
Q

discuss + explain the hypothalamic pituitary adrenal (HPA) axis

A
  1. The HPA axis is our central stress response system
  2. The HPA axis is responsible for the neuroendocrine adaptation component of the stress response
  3. hypothalamus releases corticotropin-releasing hormone. CRH binds to CRH receptors on the anterior pituitary gland → adrenocorticotropic hormone (ACTH) release
  4. ACTH binds to receptors on the adrenal cortex → adrenal release of cortisol
  5. At a certain blood concentration of cortisol, the cortisol exerts negative feedback to the hypothalamic release of CRF → stoppage of pituitary release of ACTH (via negative feedback loop)
  6. systemic homeostasis returns
48
Q

discuss Na+ balance in DKA/HHS

A
  1. Hyperglycemia causes osmotic shifts of water from the intracellular to the extracellular space, causing a relative dilutional hyponatremia.
  2. You gotta correct for this with the sodium correction in hyperglycaemia equation. Use the one on MDCalc, cause who has the time to remember that shit lets be honest
  3. based on Na (corrected): if Na < 145 use Nsaline
    based on Na (corrected): if Na ≥ 145 use half Nsaline
  4. based on glucometer: if glucose ≤ 14 then use D5 halfNsaline (regardless of Na)
  5. switch back and forth between solutions as indicated by Na (corrected) and/or gluc (q1h)
  6. if you correct the sodium too fast you will cause osmotic demyelination syndrome and fuck up their head
49
Q

primary vs secondary hyperthyroid

A
  1. primary is related directly to the thyroid gland itself producing too much exogenous T3 + T4
  2. secondary is related to the pituitary gland secreting too much TSH
50
Q

cushing’s syndrome

A
  1. Loss of HPA regulation leads to disorder of cortisol excess.
  2. collection of signs and symptoms due to prolonged exposure to glucocorticoids such as cortisol
  3. Cushing’s syndrome may result from any cause of increased glucocorticoid levels, whether due to medication or internal processes
  4. The most common cause of Cushing’s syndrome is the use of prescribed glucocorticoids to treat other diseases
  5. Endogenous Cushing’s syndrome results from some derangement of the body’s own system of cortisol secretion

CCP Semester 2: The Path Of Shame (20 decks)

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