Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Damjanov > Flashcards

Damjanov Flashcards

1
Q

Define precision/reliability of a test

A

Determined by repeating the same test on the same sample

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define accuracy of a test

A

Reflectts how close measured value is to the true value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define specificity; sensivity

A

True negative: [TN/(TN + FP)] x 100;

True positive: [Tp/(TP + FN)] x 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define positive and negative predictive value; define EFFICIENCY!

A

Pos: [TP/(TP + FP)] x 100;
Neg: [TN/(TN + FN)] x 100;
[(TP + TN)/(TP + TN + FP + FN)] x 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the most important electrolyte in the ECV? ICV?

A

Na; K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

For Na, list the percentages where it’s distributed, what makes up the exchangeable sodium, and what the serum concentration of Na normally is

A

50% in ECF, 40% in bone, 10% inside cells;
made up by all Na in EC and IC fluid and approx 50% in bone;
135-145 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is most Na excreted? Where else is it lost? How is sodium controlled?

A

Through the urine; some lost in feces and sweat;

  1. Thirst (osmoreceptors in hypothalamus can increase osmolality of plasma if too much sodium ingested or water lost)
  2. ADH (if water lost and osmolality increases, ADH stimulates water reabsorption of water in kidney; depletion of intravascular volume can stimulate thirst and ADH)
  3. Aldosterone: Lose ECV, affects GFR; renin released from juxtaglomerular apparatus, and through RAA aldosterone promotes Na and K/H exchange in distal renal tubules
  4. ANP: stimulates kidneys to increase Na excretion in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the three main physiologic processes Na participates in?

A
  1. Acid-base balance: binds to anions like phos, chloride, bicarb
  2. Cell membrane polarity: sodium helps contribute to formation of electric charges across cell membranes; ATPase helps move it out of cell
  3. Osmolality of body fluids: essential for body fluid osmolality maintenance; if ECF slightly increased, osmoreceptors stimulated, and thirst, ADH release, and water reabsorption in kidneys initiated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Calc serum osmolality; what is an osmolality gap?

A

Serum osmolality = 2 x Na + (glucose/18) + (BUN/2.8);

measured and observed osmolality discrepancy, usually caused by something like alcohol or ethylene glycol in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define hyponatremia; what are the two types? List them!

DISRS vs. GRD

A

Serum osmolality < 136 mmol/L;
1. Dilutional
A. Increased water intake (polydipsia, infusion)
B. SIADH
C. Reduced water excretion (heart failure, hepatorenal syndrome, renal disease)
D. Shift of water to ECV (diabetes, multiple myeloma, hyperlipidemia)
E. Hypoproteinemia (cirrhosis, malnutrition, nephrotic syndrome)
2. Depletion
A. GI loss (vomiting, diarrhea, GI fistula, ileus)
B. Renal loss (salt wasting, diuretics, osmotic diuresis, Addison’s disease)
C. Dermal loss (burns)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the four broad reasons for why hyponatremia occurs? How should treatment of hyponatremia be directed?

A
  1. Increased total body H2O
  2. Relative increase of H2O in ECV
  3. Reduced total body salt and water (Na > H2O)
  4. Increased total body H2O and salt (H2O > Na);
    Correction of Na-H2O balance and the hyponatremia causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is hypernatremia defined? What are the body’s compensations? What can cause hypernatremia? (4 major categories)

A

> 150 mmol/L; increased water intake or water conservation through kidneys, and ADH release;
1. Decreased intake of H20 (Lack of drinking water, unconscious)
2. Increased loss of H2O
A. Kidney (diabetes mellitus, insipidus, nephrogenic diabetes insipidus)
B. Skin (sweating)
C. GI (diarrhea)
3. Retention of Na (Conn’s and Cushing’s, corticosteroids)
4. Infusion of Na (Medical: Na2CO3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Symptoms of hypernatremia? TOIRCAM, HTRL

A

Thirsty, oliguria, irritability, restlessness, confusion, agitation, muscle weakness;
hypotension, tachycardia, renal failure due to hypoperfusion, lethargic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the major anion of plasma and interstitial fluids? Reference range for chloride? When would its metabolism differ from Na?

A

Cl; 98-106 mmol/L;
Hyperchloremic metabolic acidosis (depletion of HCO3 leads to Cl replenishment)
Hypochloremic metabolic alkalosis (Cl lost in GI tract leads to metabolic alkalosis, with anion gap filled with bicarb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the principal IC cation? Where is most of it found? Reference range? What two factors regulate K excretion? What promotes K secretion into the distal tubule, and what other ion(s) can move?

A

K; 98% inside cells, 2% in ECF; 90% of IC K is in exchangeable IC pool, and 8% structurally bound to bone, brain cells, and RBC’s;
3.5-5;
Concentration of K in blood and GFR;
aldosterone, with reabsorption of Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is renal acidosis associated with? What about renal alkalosis? Excess of H favors exchange of ____ for ____? What can promote K flux across the cell membrane, and what might favor efflux of K from cells?

A

Hyperkalemia; hypokaelmia; Na, H;

Insulin, diabetes (due to lack of insulin

17
Q

What causes hypokalemia? (4 broad categories)

A
  1. Low intake of K (starvation, anorexia nervosa, alcoholism)
  2. GI loss of K (vomiting, diarrhea, fistula, laxatives)
  3. Renal loss of K
    A. Diuresis –> (diabetes, diuretics)
    B. Hyperaldosteronism and Cushing’s –> (Na retention)
    C. Tubular dysfunction –> (End-stage kidney)
  4. Redistribution of K (alkalosis, insulin, familial periodic muscle paralysis)
18
Q

Consequences of hypokalemia? CNGM

A
  1. Cardiac: arrythmia and abnormal cardiac contractions with ECG changes
  2. Neuromuscular: generalized muscle weakness and hypotonia; lethargy, depression, confusion
  3. GI: slow peristalsis leading to ileus or constipation
  4. Metabolic/renal: alkalosis and polyuria
19
Q

What leads to hyperkalemia? (5 categories) A consequence of hyperkalemia and subsequent treatment?

A
  1. Excessive intake (oral supplements, infusion)
  2. Decreased Renal excretion (End-stage renal failure, minteralcorticoid deficiency, Addison’s, K-sparing diuretics)
  3. Redistribution of ICV to ECV (acidosis)
  4. Massive cell injury (burns, crush injury, rhabdomyolysis)
  5. Tumor lysis syndrome (chemo);
    cardiac arrhythmias: ventricular arrhythmia and then v fib, so treat with calcium gluconate and then hypertonic glucose
20
Q

Normal blood has H concentration of ______ and pH of _____; what two things account for blood’s buffering capacity? When H ions enter the urine, they are linked to ______ and ______;

A

40; 7.4; Hg and bicarb;

phosphate and ammonia

21
Q

What does metabolic acidosis result from? How does compensation occur? What causes metabolic acidosis (two broad categories with 4 subcategories each)? DEKALS

A

Loss of bicarbs and increased concentration of H ion in ECF; decreased pH of arterial blood stimulates central chemoreceptors, provoking hyperventilation;
1. Acidosis with normal anion gap
A. GI loss of bicarbs (diarrhea; GI, biliary or pancreatic fistulae)
B. Renal diseases (obstructive uropaty, renal tubular acidosis, chronic pyelonephritis)
C. Hypoaldosteronism
D. Hyperalimentation

  1. Acidosis with normal anion gap
    A. Ketoacidosis (diabetes, alcohol abuse)
    B. Lactic acidosis (tissue damage and ischemia, liver insufficiency)
    C. End-stage kidney disease
    D. Poisoning (salicylates, ethylene glycol, methanol)
22
Q

Define the anion gap; what is the normal value?

A

Na + K - (Cl +CO2); 10 - 20 mmol/L

23
Q

Causes of metabolic alkalosis? 3 broad categories

A
  1. Gastric H loss (vomiting, gastric drainage)
  2. Renal H loss and HCO3 retention (hyperaldosteronism: Conn’s and Cushing’s if primary, renal hypertenion if secondary; hypokalemia: diuretics, chronic diarrhea; volume contraction (cirrhosis)
  3. Net gain of HCO3 (absorbable antacids: milk alkali syndrome; ingestion of bicarb: baking soda)
24
Q

What is respiratory acidosis characterized by? What about respiratory alkalosis?

A

Retention of CO2 due to hypoventilation; hyperventilation, leading to increased loss of CO2

25
Q

What contains most of the total body Ca? What does the rest of the Ca help make up? What controls the metabolic processes of absorption in intestine, excretion through kidneys, and balance with calcium stores in bones? For the protein-bound Ca (40-50%), what is it mostly bound to?

A

Bones (99%); exchangeable Ca pool (plasma, ECF, ICF: 1%);
PTH, calcitonin, vit D, thyroxin, cortisol, growth hormone;
80% albumin, 20% globulin

26
Q

When do we see more Ca bound to proteins? What acts as trigger of PTH release? What could lead to pseudohypocalcemia?

A

Alkalosis, dehydration, paraproteinemia; concentration of Ca; hypoalbuminemia

27
Q

To determine if there is hypocalcemia associated with hyperphosphatemia or hypophos, what tests could be done? What are the subgroups of these types of hypocalcemias? 3 and 5 respectively

A

Serum levels of Mg, calcitriol (Vit D), PTH;
A. with hyperphos
1. hypoparathyroidism (like DiGeorge or after surgery)
2. Chronic renal failure (phosphate retention and inadequate hydroxylation of vit D: measure with serum PTH, measure serum BUN and creatine, or measure vit D)
3. hypomagnesemia (Mg essential to form active PTH)

B. hypophos

  1. Inadquate intake of Vit D
  2. Rickets
  3. Intestinal malabsorption
  4. Renal or liver disease
  5. Drug-related
28
Q

What other causes could cause hypocalcemia in general?

A
  1. Hypocalcemia of acute onset (acute necrosis of pancreas due to saponification)
  2. Neonatal hypocalcemia (inborn errors of metabolism with hyperphos, pseudohyperPTH, vit D 1alpha-hydroxylase deficiency)
29
Q

What are symptoms of hypocalcemia?

A
  1. Neuromuscular (numbness, paresthesia, muscle spasm: Chvostek’s sign is facial spasm, Trousseau’s is carpal spasm)
  2. Cardiac (prolonged QT interval)
  3. Behavioral (lack of alertness, convulsions, LOC)
  4. Laryngeal stridor
30
Q

Causes of hypercalcemia? 7 things

A
  1. Primary hyperparathyroidism, 2, 3
  2. Malignant tumors (direct bone destruction or action of osteolytic hormones and cytokines)
  3. PTHrP (excretion of Ca in urine increased, low PTH)
  4. Multiple myeloma and lymphomas (IL-1 and TNF secreted and osteoclasts activated and bone trabeculae lysed)
  5. Vit D-related hypercalcemia with hypervitaminosis D
  6. Granulomatous diseases (sarcoid, TB, fungal)
  7. Hyperthyroidism
31
Q

Symptoms of hypercalcemia? 5 things

A
  1. Renal symptoms: polyuria, renal stones, renal damage
  2. CNS: fatigue, apathy, depression, coma
  3. Musculoskeletal: bone pain, osteoporosis, fractures, muscle weakness
  4. GI: anorexia, pain, constipation, peptic ulcer, pancreatitis
  5. Cardiovascular: ECG changes, arrhythmia, cardiac arrest
32
Q

How do Ca and P relate? How much of filtered phosphate is reabsorbed?

A

Reciprocal relationship: hypercalcemia means hypophosphatemia; There is a reciprocal relationship; 95% of the filtered phosphate is reabsorbed in the prox tubule

33
Q

Causes of hypophos? 3 things

A

A. Reduced absorption and intake (chronic malnutrition, chronic alcoholism, abuse of phosphate-binding antacids)
B. Increased Loss/Removal (HyperPTH, vit D deficiency, hemodialysis, peritoneal dialysis)
C. Shifts of Phosphates from EC to IC space
1. Insulin and carb metabolism (infusion of glucose or insuline, treatment of diabetic acidosis, nutritional recovery, hyperalimentation, severe burns)
2. Alkalosis (respiratory alkalosis, bicarb infusion)
3. EC fluid volume expansion

34
Q

What causes hyperphosphatemia? What are three major consequences of this?

A

A. Pseudohyperphosphatemia (blood hemolysis, multiple myeloma)
B. Increased intake (rectal phosphate enema, IV phosphate)
C. Cell lysis (tumor lysis syndrome, rhabdo, heat stroke, hepatic necrosis, severe hemolytic anemia)
D. Diminished excretion (renal failure)

  1. Hypocalcemia (tetany, spastic skeletal muscle contraction)
  2. Metastatic calcification (calcium phosphate is insoluble)
  3. Calciphylaxis
35
Q

Regarding albumin, where is it made and how is it lost?

A

Made in the liver; decreased synthesis by liver or increased loss through kidneys, intestines, or external body surface

36
Q

List the alpha1, alpha2, beta, and gamma globulins

A 
Alpha1: alpha1-antitrypsin (serine protease inhibitor) and alpha-FP (seen in liver cell carcinoma, gonadal tumors, and Down syndrome)
Alpha2: alpha2-macroglobulin (protease inhibitor with increased concentration in nephrotic syndrome), haptoglobin (binds free Hb), ceruloplasmin (transports iron and copper, decreased in Wilson's disease)
Beta: transferrin (major iron-transporting protein, reduced in chronic anemia), complement factors C3 and C4 (reduced in autoimmune disorders), beta2-microglobulin (light-chain portion of class I HLA expressed on blood cells and tissue cells, but increased in patients with B-cell lymphoma, leukemia, or multiple myeloma)
Gamma: five classes of immunoglobulins, also C-reactive protein (use for monitoring infectious diseases, chronic conditions like rheumatoid, and rejection of transplanted organs, angina pectoris)
37
Q

List the enzymes that increase and the elevated concentration of certain markers in the serum

A
  1. Aminotransferases (AST and ALT, with AST mostly in liver mito, and ALT ONLY in cytosol)
  2. Alkaline phosphatase (could be increased in osteoblastic tumors or in biliary obstruction)
  3. LDH (neoplastic states, cell lysis, tissue injury)
  4. CK: Found in skeletal and striated muscle, coming out as CK-MM, CK-MB, and CK-BB
38
Q

What are the ranges of lipoprotein levels?

A

Triglycerides: 40-160 mg/dL in men, 35-135 mg/dL in women
Total cholesterol: below 200 mg/dL
LDL below 100 mg/dL
HDL over 60 mg/dL

Pathology (40 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions