Clin Med- (electrolytes)Approach to CP, SOB/DOE, Palpations Flashcards
What triggers ADH release?
- Osmotic stimuli–> from increases in serum osmolarity detected by osmoreceptors
- Non-osmotic stimule - decreases in BP or Blood volume detected by Baroreceptors
What are non osmotic stimuli for ADH release?
- Baroreceptors
- Nausea
- Hypoxia
- Pain
- Meds (opiates, antidepressants)
- pregnancy
what sodium level are symptomatic for hyponatriemia?
less than 125 mEq/L
What is considered acute hyponatriemia?
less than 48 hours
What are hypovolemic exam findings?
-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
What are hypervolemia exam findings?
- HTN
- Sacral or LE edema
- JVD
- Dilated IVC on echo
How do you diagnose SIADH?
Diagnosis of exclusion:
Must rule out
-cortisol deficiency
- hypothyroidism,
- other causes
What is the most common malignancy associated with SIADH?
Small cell lung cancer
What drugs can cause SIADH?
COMAAA
- Cyclophosphamides
- Opiates
- MDMA (ecstasy)
- Antidepressants
- Anticonvusants
- Antipsychotics
What are concerns of acute hyponatremia (<48 hours) correction?
Can be corrected rapidly with little risk of osmotic demyelination syndrom
How should you treat chronic hyponatremia?
- raise serum Na by 8-10 mEq/day
2. Do not raise more than 18 mEq/L in the first 48 hours
How should you treat symptomatic hyponatremia patients?
Give hypertonic saline (3%) to quickly raise sodium until no longer sx (3-4 mEq/L) then continue to raise slowly
What do you do if sodium is over corrected?
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
What are complications of hyponatremia?
-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
Where does demyelination occur in Osmoticdemylination syndrome ODS? When do you see it?
- demyelination in the pontine and extrapontine neurons
- clinical manifestations are typically delayed fro 2-6 days after rapid Na+ correction
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
Osmotic demyelination syndrome
What concentration is considered hypernatremic?
> 145mEq/L
Risk factors for what include: -Trauma – Burns – ICU patients – Dementia – Uncontrolled diabetes, etc...
Hypernatremia
What are 2 processes that can cause hypernatremia?
- Unreplaced water loss (dehydration)
- GI, renal , impaired thirst, burns etc
- Sodium overload
– 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?
Hypernatremia
What is goal in chronic hypernatremia tx?
lower Na+ by 10-12mEq/L per day
any more puts them at risk for cerebral edema
What are 2 steps in treated hypernatremia?
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
What sites of the nephron are primarily responsible for K+ regulation?
Cells in the distal lumen
1. Principal cells SECRETE K+ in Collecting duct (also respond to ADH via V2 receptor)
- Alpha intercalated cells in the collecting duct REABSORB K+
What serum potassium concentration is considered hyperkalemia?
> 5.0 or 5.5 mEq/L
– AKI – CKD – Diabetes mellitus – Medications (NSAIDs, ACEi/ARB, Aldosterone antagonists, heparin, etc...) – Malignancy (TLS) – Rhabdomyolysis – Older age – Acidosis
Are risk factors for what?
Hyperkalemia- affects up to 10% of hospitalized patients
What are clinical manifestations of Hyperkalemia?
- Cardiac arrhythmia - V fib, Brady cardia, asystole
- wide QRS, peaked T wave
- Skeletal muscle weakness -> respiratory failure from diaphragm weakness
- Metabolic Acidosis -> K+ enters and H+ leaves to maintain electroneutrality; Hyperkalemia decreases ammonia genesis-> decreases ammonium chloride excretion
How doe hyperkalemia affect resting membrane potential?
initial -> hyperexcitability
long term -> inactivates sodium channels, decreases membrane excitability, impairs cardiac conduction and/or neuromuscular weakness
What are 2 main reasons for hyperkalemia?
- transcellular shift out of cells
2. decreased renal excretion
What Is the pathogenesis of hyperkalemia from transculluar shift?
- Pseudo hyperkalemia
- metabolic acidosis
- insulin deficiency, hyperglycemia, hyperosmolality (insulin stimulates Na/K pump to drive K+ intracellularly) (hyperglycemia causes H2O to leave cells and takes K+ with it)
- Tissue catabolism release K+ (tumor lysis, trauma, burns, radiation
- Meds (BB, a1 agonist, digoxin, succinylcholine)
- Exercise
- Blood transfusion
What causes hyperkalemia from decreased renal K+ excretion?
- Low aldosterone secretion (can be meds)
- Aldosterone resistance ( potassium sparing diuretics)
- AKI or CKD from low GFR
How do you treat hyperkalemia?
- Calcium glutinate for peaked T eaves
- insulin and dextrose for transcellular shift
- diuretic or exchange resin for potassium removal
- low K+ diet
- discontinue ACEi, ARB, Aldosterone blocker
What concentration defines hypokalemia?
<3.5mEq/L K+ (symptomatic at <3.0)
Diarrhea, vomiting, meds(insulin, diuretics) are risk factors for what?
Hypokalemia
What are clinical sx of hypokalemia?
- Cardiac arrhythmia (PAC, PVC, tachycardia, Brady cardia, v fib)
- Skeletal muscle weakness (including diaphragm
- Rhabdomyolysis
- Metabolic Alkalosis -> K+ moves from ICF to ECF leading to H+ uptake
- Nephrogenic diabetes insipidus
What does hypocalcemia show on ECG?
prominent U wave and flat T wave
What are 3 main causes of hypokalemia?
- Transcellular Shift (increase K+ uptake)
- External loss ( GI loss, sweat)
- Renal loss
What can cause hypokalemia via transcelluar shift?
- Insulin
- B2 agonist
- Metabolic alkalosis
What causes hypokalemia via extra renal loss?
- GI loss (vomiting, NG suction, diarrhea)
2. Cutaneous losses - sweating
What causes hypokalemia via renal losses?
- Diuretics
- Increased mineralocorticoid activity (Conn’s or Cushing’s syndrome)
- Hypomagnesemia
- RTA type 1 or 2
- Intrinsic renal defect (Bartter, Gitleman, Liddle)
