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CPR Final > Clin Med- (electrolytes)Approach to CP, SOB/DOE, Palpations > Flashcards

Clin Med- (electrolytes)Approach to CP, SOB/DOE, Palpations Flashcards

1
Q

What triggers ADH release?

A
  1. Osmotic stimuli–> from increases in serum osmolarity detected by osmoreceptors
  2. Non-osmotic stimule - decreases in BP or Blood volume detected by Baroreceptors
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2
Q

What are non osmotic stimuli for ADH release?

A
  1. Baroreceptors
  2. Nausea
  3. Hypoxia
  4. Pain
  5. Meds (opiates, antidepressants)
  6. pregnancy
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3
Q

what sodium level are symptomatic for hyponatriemia?

A

less than 125 mEq/L

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4
Q

What is considered acute hyponatriemia?

A

less than 48 hours

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5
Q

What are hypovolemic exam findings?

A

-HTN
-Orthostatic vital signs
-tachycardia
-poor capillary refill
-increased skin turgor
- dry oral mucosa, skin fissuring
- Flat JV
hx of decreased urea
- more than 50% collapsed JVD on echo

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6
Q

What are hypervolemia exam findings?

A
  • HTN
  • Sacral or LE edema
  • JVD
  • Dilated IVC on echo
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7
Q

How do you diagnose SIADH?

A

Diagnosis of exclusion:
Must rule out
-cortisol deficiency

  • hypothyroidism,
  • other causes
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8
Q

What is the most common malignancy associated with SIADH?

A

Small cell lung cancer

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9
Q

What drugs can cause SIADH?

A

COMAAA

  1. Cyclophosphamides
  2. Opiates
  3. MDMA (ecstasy)
  4. Antidepressants
  5. Anticonvusants
  6. Antipsychotics
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10
Q

What are concerns of acute hyponatremia (<48 hours) correction?

A

Can be corrected rapidly with little risk of osmotic demyelination syndrom

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11
Q

How should you treat chronic hyponatremia?

A
  1. raise serum Na by 8-10 mEq/day

2. Do not raise more than 18 mEq/L in the first 48 hours

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12
Q

How should you treat symptomatic hyponatremia patients?

A

Give hypertonic saline (3%) to quickly raise sodium until no longer sx (3-4 mEq/L) then continue to raise slowly

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13
Q

What do you do if sodium is over corrected?

A

If serum sodium correction is too fast, you need to lower sodium back an acceptable level to prevent ODS:

  • 5% Dextrose in Water (D5W), a.k.a free water
  • DDAVP
  • D5W and DDAVP
  • Discontinuation of some therapies that are raising sodium
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14
Q

What are complications of hyponatremia?

A 
-Osteoporosis
• Falls
• Seizures
• Coma
• Death from brain (uncal) herniation
• Osmotic demyelination syndrome (ODS)
– Previously called central pontine myelinolysis (CPS)
• Occurs with rapid serum Na+ correction in chronic hyponatremia
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15
Q

Where does demyelination occur in Osmoticdemylination syndrome ODS? When do you see it?

A
  • demyelination in the pontine and extrapontine neurons

- clinical manifestations are typically delayed fro 2-6 days after rapid Na+ correction

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16
Q 
Symptoms of what are often irreversible or only partially reversible:
– Dysarthria
– Dysphagia
– Paraparesis or quadriparesis
– Behavioral disturbances
– Pseudobulbar palsy
– Seizures
– Lethargy
– Confusion
– Coma
• Some will develop Locked-in syndrome, meaning they are awake but unable to move or communicate – Death
A

Osmotic demyelination syndrome

17
Q

What concentration is considered hypernatremic?

A

> 145mEq/L

18
Q 
Risk factors for what include:
-Trauma
– Burns
– ICU patients
– Dementia
– Uncontrolled diabetes, etc...
A

Hypernatremia

19
Q

What are 2 processes that can cause hypernatremia?

A
  1. Unreplaced water loss (dehydration)
    • GI, renal , impaired thirst, burns etc
  2. Sodium overload
20
Q 
– Irritability
– Altered mental status
– Lethargy
– Ataxia
– Seizures
– Hyperreflexia
– Intracerebral hemorrhages, Subarachnoid hemorrhages, or Subdural hematomas
• Result from rapid brain cell shrinkage

are sx of what?

A

Hypernatremia

21
Q

What is goal in chronic hypernatremia tx?

A

lower Na+ by 10-12mEq/L per day

any more puts them at risk for cerebral edema

22
Q

What are 2 steps in treated hypernatremia?

A

1.Replace the water deficit
• 5% Dextrose in Water (D5W), a.k.a free water
• Other hypotonic solutions (1/2 NS, etc…)

2.Correct underlying cause leading to water loss

23
Q

What sites of the nephron are primarily responsible for K+ regulation?

A

Cells in the distal lumen
1. Principal cells SECRETE K+ in Collecting duct (also respond to ADH via V2 receptor)

  1. Alpha intercalated cells in the collecting duct REABSORB K+
24
Q

What serum potassium concentration is considered hyperkalemia?

A

> 5.0 or 5.5 mEq/L

25
Q 
– AKI
– CKD
– Diabetes mellitus
– Medications (NSAIDs, ACEi/ARB, Aldosterone antagonists, heparin, etc...)
– Malignancy (TLS)
– Rhabdomyolysis
– Older age
– Acidosis

Are risk factors for what?

A

Hyperkalemia- affects up to 10% of hospitalized patients

26
Q

What are clinical manifestations of Hyperkalemia?

A
  1. Cardiac arrhythmia - V fib, Brady cardia, asystole
    • wide QRS, peaked T wave
  2. Skeletal muscle weakness -> respiratory failure from diaphragm weakness
  3. Metabolic Acidosis -> K+ enters and H+ leaves to maintain electroneutrality; Hyperkalemia decreases ammonia genesis-> decreases ammonium chloride excretion
27
Q

How doe hyperkalemia affect resting membrane potential?

A

initial -> hyperexcitability

long term -> inactivates sodium channels, decreases membrane excitability, impairs cardiac conduction and/or neuromuscular weakness

28
Q

What are 2 main reasons for hyperkalemia?

A
  1. transcellular shift out of cells

2. decreased renal excretion

29
Q

What Is the pathogenesis of hyperkalemia from transculluar shift?

A
  1. Pseudo hyperkalemia
  2. metabolic acidosis
  3. insulin deficiency, hyperglycemia, hyperosmolality (insulin stimulates Na/K pump to drive K+ intracellularly) (hyperglycemia causes H2O to leave cells and takes K+ with it)
  4. Tissue catabolism release K+ (tumor lysis, trauma, burns, radiation
  5. Meds (BB, a1 agonist, digoxin, succinylcholine)
  6. Exercise
  7. Blood transfusion
30
Q

What causes hyperkalemia from decreased renal K+ excretion?

A
  1. Low aldosterone secretion (can be meds)
  2. Aldosterone resistance ( potassium sparing diuretics)
  3. AKI or CKD from low GFR
31
Q

How do you treat hyperkalemia?

A
  1. Calcium glutinate for peaked T eaves
  2. insulin and dextrose for transcellular shift
  3. diuretic or exchange resin for potassium removal
  4. low K+ diet
  5. discontinue ACEi, ARB, Aldosterone blocker
32
Q

What concentration defines hypokalemia?

A

<3.5mEq/L K+ (symptomatic at <3.0)

33
Q

Diarrhea, vomiting, meds(insulin, diuretics) are risk factors for what?

A

Hypokalemia

34
Q

What are clinical sx of hypokalemia?

A
  1. Cardiac arrhythmia (PAC, PVC, tachycardia, Brady cardia, v fib)
  2. Skeletal muscle weakness (including diaphragm
  3. Rhabdomyolysis
  4. Metabolic Alkalosis -> K+ moves from ICF to ECF leading to H+ uptake
  5. Nephrogenic diabetes insipidus
35
Q

What does hypocalcemia show on ECG?

A

prominent U wave and flat T wave

36
Q

What are 3 main causes of hypokalemia?

A
  1. Transcellular Shift (increase K+ uptake)
  2. External loss ( GI loss, sweat)
  3. Renal loss
37
Q

What can cause hypokalemia via transcelluar shift?

A
  1. Insulin
  2. B2 agonist
  3. Metabolic alkalosis
38
Q

What causes hypokalemia via extra renal loss?

A
  1. GI loss (vomiting, NG suction, diarrhea)

2. Cutaneous losses - sweating

39
Q

What causes hypokalemia via renal losses?

A
  1. Diuretics
  2. Increased mineralocorticoid activity (Conn’s or Cushing’s syndrome)
  3. Hypomagnesemia
  4. RTA type 1 or 2
  5. Intrinsic renal defect (Bartter, Gitleman, Liddle)

CPR Final (2 decks)

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