Patho Exam 3 part 3 Flashcards
1
Q
Potassium
- where stored?
- physiologic role?
A
Potassium
- most abundant cation
1. 98% of total body stores are intracellular - Muscle: 75%
- Liver and RBCs: 25%
- Physiologic role
- Cell metabolism
- -protein and glycogen synthesis
- membrane potential
- -cardiac and neuromuscular tissue
- cardivascular health
- -blood presure balance
- -stroke prevention
2
Q
Potassium Homeostasis
-Diet?
A
Potassium Homeostasis
- Abundant in fruits, vegetables, and meat
- Recommended intake: 50mEq/day
- cardiovascular health: 100mEq/day
- easily and extensively absorbed
3
Q
Potassium Homeostasis
-Renal Elimination?
A
Potassium Homeostasis
- freely filtred in bowmans capsule
- Almost entirely absorbed passively in proximal tubule and thick ascending limb
- 80% of daily intake eliminated
4
Q
Potassium Homeostasis
-GI Elimination?
A
Potassium Homeostasis
- GI Elimination
- Mostly absorbed
- amonted excreted via feces increased with diarrhea and CKD
5
Q
Hormones
-insulin?
A
Hormones
- Insulin
- stimulates shit of potassium intracellularly via NA/K ATPase pump.
- -Liver, adipose, muscle
6
Q
Hormones
-catecholamines?
A
Hormones
- .AKA epinephrine
1. stimulate beta-receptors. - activate NA/K ATPase pump
2. stimulate glycogenolysis - increase blood glucose stimulating insulin secretion activating NA/K ATPase pump
7
Q
Hormones
-Aldosterone?
A
Hormones
- Aldosterone
- stimulates sodium reabsorption and potassium excretion in distal tubule and collecting duct
8
Q
Fluid Tonicity
-Hyperosmolarity
what is it?
A
Hyperosmolarity
- fluid shift intracellular to extracellular
- increases intracellular:extracellular potassium gradient
- shifts potassium extracellularly
9
Q
Hypokalemia
-types due to serum potassium?
A
Hypoalemia
- Serum potassium < 3.5 mEq/L
- Mild: 3.1 - 3.4 mEq/L
- Mod: 2.5-3.0 mEq/L
- Severe: <2.5 mEq/L
-total body deficit versus shift from extracellular to intracellular compartmnet
10
Q
Hypokalemia
-Total body deficit Etiology?
A
Hypokalemia
- Total body deficit
- Decreased intake
- -uncommon
- -risk factors
- –elderly with chronic conditions
- –surgery
- Increased elimination
- -excessive renal or GI losses
11
Q
Hypoalkemia
-Excessive renal losses Etiology?
A
Hypokalemia
- Most common cause of hypoalemia
- Drug-induced
- Diuretics
- High dose penicillin
- mineralocorticoid (Dexamethasone, fludrocortisone)
- amphotericin
- cisplatin
12
Q
Hypoalkemia
-Excessive GI losses etiology?
A
- Diarrhea and/or vomiting
- Direct loss
- loss of bicarbonate (causing metabolic alkalosis which then shifts K+ intracellularly)
- Drug-induced
- -Sorbitol
- -sodium polystyrene sulfonate
13
Q
Hypoalemia: Etiology
-Co-existing hypomagnesmia?
A
- similar causes
- hypomagnesemia promotes renal potassium wasting
14
Q
Hypokalemia: Clinical presentation
- symptoms?
- mod symtoms?
- severe symptoms?
A
- variable, depends on degree of hypokalemia
- asymptomatic
- mod: cramping, muscle aches, malaise, myalgias
- sev:
1. EKG chanages: ST-segment depression or flattening, T-wave inversion - Heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation
15
Q
Hyperkalemia: Clinical Presentation
- mild?
- mod?
- Sev?
A
- Serum potassium > 5 mEq/L
- Mild: 5.1-5.9 mEq/L
- Mod: 6-7 mEq/L
- Severe: >7 mEq/L
16
Q
Hyperkalema: Etiology
- relation to hypokalemia?
- causes?
A
- Less common than hypokalemia
- Usually results from overcorrection of hypokalemia
1. Four mains causes - Increased Intake
- Decreased Excretion
- Tubular unresponsiveness to aldosterone
- Redistribution
17
Q
Hyperkalemia: Etiology Increased Intake
-causes?
A
- Noncompliance with low potassium diet in patients with CKD stage 4-5 and on hemodialysis
- fruits and vegatables
- salt substitutes
- herbal supplements
18
Q
Hyperkalemia: Etiology Decreased Excretion
-causes?
A
- Acute Kidney Injury
- Severe hyperkalemia more likely - CKD
- Decreased Aldosterone production
- Addison’s disease
- adrenal insufficiency
- hypoaldosteronism - Drug-induced
- Ace-Hibitors ( Lisinopril, enalapril)
- Angiotensis receptor blockers (ARBs) (Losartan, Valsartan)
- Potassium-sparing diurectics (spironolactone, amiloride)
- NSAIDS
19
Q
Hyperkalemia: Etiology Redistribution
- what is it?
- Change in body stores?
- Causes
A
- Shift from intracellular to extracellular
- No change in total body stores
1. Causes - Metabolic acidosis
- Diabetes
- Lactic acidosis
- Beta-Blockers
2. Pseudohyperalemia - Hemolysis
20
Q
Hyperkalemia: Clinical Presentation
- depends on?
- symphtoms?
A
- Depends on severity of hyperkalemia
- Asymptomatic
- Heart palpitations or skipped heart beats
- ECG changes
21
Q
Hyperkalemia: ECG Changes
A
- Tall peaked T wave
- Loss of P wave
- Widened QRS with Tall T wave
- 1-3 increases by degree of hyperkalemia
22
Q
Magnesium
- where located?
- normal serum levels?
- physiologic role?
A
- Mostly intracellular cation, second to potassium
- 1.4-1.8 mEq/L is normal level, may not reflect total Mg+ stores
- Cofactor in cellular metabolism
1. Mitochondrial Function
2. PTH Secretion
3. Glucose metabolism
23
Q
Magnesium Balance
- dietary intake?
- Renal elimination?
A
- 30-40% of ingested amount is absorbed
- more ingested –> less absorbed - Main route of elimination
- Easily filtered, but almost all (95%) reabsorbed
- -Most reabsorption occurs in thick ascending limb of loop of Henle
24
Q
Hypogmagnesmia
-Etiology - GI disorders?
A
- GI Disorders
1. Reduced intake - prolonged parenteral nutrition without supplementation
- alcoholism
2. Reduced absorption - Celiac disease, short bowel syndrome
3. Increased loss - Vomiting, excessive laxative use, prolonged diarrhea
25
Q
Hypogmagnesemia
-Etiology - Renal disorders?
A
- Renal disorders
1. Primary tubular disorders - Renal tubular acidios
- Postrenal transplant diuresis
- Diuretic phase of ATN
2. Glomerulonphritis
3. Drugs - Aminoglycosides, Amphototericin B
- Cyclosporine, tacrolimus
- Diuretics (loop)
- Digoxin
- Cisplatin
4. Hormone - Hyperthroidism
- Primary hyperparathyroidism
- Aldosteronism
26
Q
Hypogmagnesemia
-Etiology - Redistribution + Other
A
- Redistribution
- diabetic ketoacidosis
- Glucose, amino acid, or insulin administration - Other
- Excessive sweating and lactation
- Extracellular fluid volume expansion
27
Q
Hypogmagnesemia
- Clinical Presentation
1. Depends on?
2. Types + symptoms?
A
- Depends on severity of hypomagnesemia
1. Neuromuscular - Tetany
- Twitching
- Convulsions
- Tremor
2. Cardiac - Heart palpitations
- ECG changes
- -Arrhythmias (ventricular fibillation, torsade de pointes)
- -T wave change - peaked or flattened
- -Prolonged PR interval
- -widened QRS comple
- Sudden cardiac death
28
Q
Hypogmagnesemia :Clinical Presentation
- Serum level?
- Coexisting disorders?
A
- Serum level < 1.4 mEq/L
- Co-existing potassium and calcium disorders
- -Hypokalemia
- -Hypocalcemia
29
Q
Hypermagnesemia: Etiology
A
- Rare
- Patients with CKD stage 4-5 and elderly predisposed
1. Excessive intake - Cathartics
- Antacid therapy
- Treatment of eclampsia
2. Decreased renal excretion - Acute kidney injury
- CKD with exogenous intake
3. Other - Lithuum therapy
- Hypothyroidism
- Addison’s Disease
- Acute diabetic ketoacidosis
30
Q
Hypermagnesemia: Clinical presentation
- Degree?
- whats it affect?
- signs and symptoms?
A
- Depends on degree of hypermagnesemia
- > 2.3 mEq/L
- symptoms rare unless serum leves > 4 mEq/L - affects neuromuscular and cardiovascular systems
- Signs and symptoms
- Cardiac
- -Hypotension, dysrhythmias, complete heart block, aystole
- Neuromuscular
- -Sedation, muscle weakness, hyporeflexia, somnolence, coma, paralysis, respiratory depression
31
Q
Calcium
-Physiologic role?
A
- Cell membrane integrity
- Cardiac and smooth muscle activity
- Neuromuscular activity
- Secretion of endocrine and exocrine hormones
- Coagulation cascade
32
Q
Calcium
-Normal serum level?
A
- Total serum calcium
- Normal : 8.5-10.5 mg/dl - Total serum calcium = lonized (unbounded) + bounded to albumin
- Active form: ionized calcium
- Normal: 4.5-5.1 mg/dL
33
Q
Calcium
-correct for hypoalbuminemia?
A
Ca-correction (mg/dl) = Measured Ca-serum + 0.8 [4g/dL -measured albumin (g/Dl)
34
Q
Albumin
- affects of change?
- meta-alkalosis?
- meta-acidosis?
A
- Alterations in albumin concentration or binding of calcium to albumin can affect serum calcium levels
1. Metabolic alkalosis - more bound to albumin -> decreased ionized calcium
2. Metabolic acidosis - Less bound to albumin -> increased ionized calcium
35
Q
Hypocalcemia: Etiology
- common?
- Causes?
A
- Uncommon, more common in criticall ill than ambulatory patients
- Causes
1. Vitamin D deficiency - Uncommon in Western Diets
- more common with GI absorption disorders –> celiac disease, gastric surgery, small bowel syndrome, bypass, surgery, intestinal resection
2. Hypomagnesemia
3. Hungry bone syndrome - recent parathroidectomy or throidectomy
4. Drug induced - Furosemide
- Phosphorous therapy
- Calcitonin and cinacalcet
- Bisphosphonates
- Phenytoin and phenobarbital
- amphotericin, aminoglycosides, cyclosporine, cisplatin
5. Hypoparthyroidism - Autoimmune disease
- congenital defects
- iatrogenic
36
Q
Hypocalcemia: Clinical presentation
- serum calcium?
- types + symptoms?
A
- Serum calcium < 8.5 mg/dL
- depeds on acuity of decrease
1. Neuromusuclar - Tetany, muscle cramps, laryngeal cramps
2. Cardiac - Hypotension, prolonged QT, bradycardia, arrhymathias, CHF
3. Neurologic - Parestesia, memory loss, confsion, anxiety, depression
4. Dermatologic - Dry, puffy, course
- Dermatitis, eczema, psoriasis
37
Q
Hypercalcemia: Etiology
A
- Neoplasms
- Bone metastasis
- Humoral induced (ovary, kidney, lung, head, neck, lung, cervix, espohagus)
- Hyperparathyroidism
- Drug indicued
- -Thiazides, lithium, Vit D, calcium, antacids
- Other
- -Rhabdomyolysis
38
Q
Phosphorus
- where located?
- normal levels?
- physiologic role?
A
- major intracellular anion
- normal serum levels - 2.5-4.5 mg/dL
- does not refelct total body stores - Physiologic role
- cell membrane integrity
- nucleic acids
- enzymatic reaction regulation related to metabolism
- energy source (ATP)
39
Q
Phosphorous Homeostasis
- Determined by?
- Dietary intake?
- Elimination?
A
- Determined by GI tract, bone, renal tubular reabsorption
- dietary intake
- 60-80% absorbed passively and actively
- PTH, Vitamin D3 promote absorption - Elimination -Renal excretion
- Readily filtered and reabsorbed (85-90%) in proximal tubule
- PTH and Vit D promote phosphorous elimination
- Reabsorption promoted by growth hormone, insulin, and insulin-like growth factor 1
40
Q
Hypophosphatemia: Etiology
A
- Decreased GI absorption
- phosphate binders
- alcoholics
- peptic ulcer disease
- CKD - Decreased tubular reabsorption
- Hyperparathyroidism
- Burn injuries
- Acetazolamide, osmotic diuretics (mannitol)
- Gluccorticoids
- Sodium Bicarbonate - Cellular shifts
- refeeding syndrome
- -high carb, high calorie, alcoholics
- respiratory alkalosis
- dextrose, glucagon, insulin, calcitonin, cathecholamines, erythropoietics agents, anabolic steroids
41
Q
Hypophosphatemia: Clinical Presentation
- Serum level?
- reduction of?
- systems and effects?
A
- Serum level < 2.4 mg/dL
- typically symptomatic in severe cases < 1 mg/dL - Reduction of intracellular ATP and Red cell 2,3 DPG
- Neurological
- irratability, apprehension, weakness, numbness, paresthesia, confusion, seizures, coma - Cardiac
- Impaired myocardial contractility, CHF - Musculoskeletal
- Myopathy, dysphagia, ileus, rhabdomyolysis, osteomalacia
- Hematologic
- hemolysis, thrombocytopenia
42
Q
Hyperphosphatemia: Etiology
- dieaseses?
- Sources?
A
- CKD
1. Exogenous sources - phosphate therapy
- phosphate-containing laxatives
- vitamin D therapy
2. Rapid tissue catabolism - rhabdomyolysis
- -compouned by resulting AKI
- treatment of acute leukemia or lymphoma
- -tumor lysis syndrome
3. Lactic acidosis and diabetic ketoacidosis
43
Q
Hyperphosphatemia: Clinical presentation -serum level ? -complexation? -symptoms -
A
- Serum level > 4.5mg/dL
- Calcium phosphate complexation and precipitation
- arteries
- joints
- soft tissues - Nausea, vomiting, diarrhea, lethargy, seizures
- Hypocalcemia
