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Patho > Patho Exam 3 part 3 > Flashcards

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%
  1. Physiologic role
    - Cell metabolism
    - -protein and glycogen synthesis
  • membrane potential
  • -cardiac and neuromuscular tissue
  • cardivascular health
  • -blood presure balance
  • -stroke prevention
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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
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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
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4
Q

Potassium Homeostasis

-GI Elimination?

A

Potassium Homeostasis

  1. GI Elimination
    - Mostly absorbed
    - amonted excreted via feces increased with diarrhea and CKD
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5
Q

Hormones

-insulin?

A

Hormones

  1. Insulin
    - stimulates shit of potassium intracellularly via NA/K ATPase pump.
    - -Liver, adipose, muscle
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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
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7
Q

Hormones

-Aldosterone?

A

Hormones

  1. Aldosterone
    - stimulates sodium reabsorption and potassium excretion in distal tubule and collecting duct
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8
Q

Fluid Tonicity
-Hyperosmolarity
what is it?

A

Hyperosmolarity

  • fluid shift intracellular to extracellular
  • increases intracellular:extracellular potassium gradient
  • shifts potassium extracellularly
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9
Q

Hypokalemia

-types due to serum potassium?

A

Hypoalemia

  1. 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

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10
Q

Hypokalemia

-Total body deficit Etiology?

A

Hypokalemia

  1. Total body deficit
    - Decreased intake
    - -uncommon
    - -risk factors
    - –elderly with chronic conditions
    - –surgery
    - Increased elimination
    - -excessive renal or GI losses
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11
Q

Hypoalkemia

-Excessive renal losses Etiology?

A

Hypokalemia

  1. Most common cause of hypoalemia
  2. Drug-induced
    - Diuretics
    - High dose penicillin
    - mineralocorticoid (Dexamethasone, fludrocortisone)
    - amphotericin
    - cisplatin
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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
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13
Q

Hypoalemia: Etiology

-Co-existing hypomagnesmia?

A
  • similar causes

- hypomagnesemia promotes renal potassium wasting

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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
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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
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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
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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
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18
Q

Hyperkalemia: Etiology Decreased Excretion

-causes?

A
  1. Acute Kidney Injury
    - Severe hyperkalemia more likely
  2. CKD
  3. Decreased Aldosterone production
    - Addison’s disease
    - adrenal insufficiency
    - hypoaldosteronism
  4. 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
  1. Tall peaked T wave
  2. Loss of P wave
  3. 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
  1. 30-40% of ingested amount is absorbed
    - more ingested –> less absorbed
  2. 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
  1. Redistribution
    - diabetic ketoacidosis
    - Glucose, amino acid, or insulin administration
  2. 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
  1. Depends on degree of hypermagnesemia
    - > 2.3 mEq/L
    - symptoms rare unless serum leves > 4 mEq/L
  2. affects neuromuscular and cardiovascular systems
  3. 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
  1. Total serum calcium
    - Normal : 8.5-10.5 mg/dl
  2. Total serum calcium = lonized (unbounded) + bounded to albumin
  3. 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
  1. 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
  1. major intracellular anion
    - normal serum levels - 2.5-4.5 mg/dL
    - does not refelct total body stores
  2. 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
  1. Determined by GI tract, bone, renal tubular reabsorption
  2. dietary intake
    - 60-80% absorbed passively and actively
    - PTH, Vitamin D3 promote absorption
  3. 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
  1. Decreased GI absorption
    - phosphate binders
    - alcoholics
    - peptic ulcer disease
    - CKD
  2. Decreased tubular reabsorption
    - Hyperparathyroidism
    - Burn injuries
    - Acetazolamide, osmotic diuretics (mannitol)
    - Gluccorticoids
    - Sodium Bicarbonate
  3. 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
  1. Serum level < 2.4 mg/dL
    - typically symptomatic in severe cases < 1 mg/dL
  2. Reduction of intracellular ATP and Red cell 2,3 DPG
  3. Neurological
    - irratability, apprehension, weakness, numbness, paresthesia, confusion, seizures, coma
  4. Cardiac
    - Impaired myocardial contractility, CHF
  5. 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
  1. Serum level > 4.5mg/dL
  2. Calcium phosphate complexation and precipitation
    - arteries
    - joints
    - soft tissues
  3. Nausea, vomiting, diarrhea, lethargy, seizures
  4. Hypocalcemia

Patho (5 decks)

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