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Patho > Comprehensive Final > Flashcards

Comprehensive Final Flashcards

1
Q

ISOTONIC FLUID LOSS

A

causes hypovolemia (decreased volume in blood)

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2
Q

Causes of isotonic fluid loss

A

Flu, heaving sweating, and hemorrhage, severe wound drainage, inadequate fluid intake

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3
Q

S/S of isotonic fluid loss

A

Very dry, weight loss, and increased HR, flattened neck veins, normal or decreased BP

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4
Q

ISOTONIC FLUID EXCESS

A

causes hypervolemia (increased volume in blood)

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5
Q

Causes of isotonic fluid excess

A

heart/renal failure, excess administration of IV fluids, hypersecretion of aldosterone (too much salt) or drugs (cortisone)

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6
Q

S/S of isotonic fluid excess

A

Weight gain, JVD, Bounding pulse, and increases BP, neck veins distended, edema

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7
Q

Describe the physiological mechanisms (and related causes) contributing to the formation of edema.

A
  1. Increased capillary hydrostatic pressure: result of venous obstruction/Na and H2O retention (Thrombophlebitis, hepatic obstruction, tight clothing around the extremities, and prolonged standing)
  2. Decreased capillary oncotic pressure: due to loss of plasma albumin production
  3. Increase in capillary permeability: due to inflammation and immune responses
  4. Lymph Obstruction
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8
Q

Hypernatremia

A

Causes: occurs with serum sodium levels exceed 145 mEq/L. Increased levels may be caused by retention of sodium or by increase loss of water. Sodium is found largely in ECF so increased sodium concentration causes intracellular dehydration.

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9
Q

S/S of hypernatremia

A

hyperosmolarity, dehydration, headache, thirst, elevated temperature, concentrated. Symptoms of hypovolemia include tachycardia, weak pulses, postural hypotension

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10
Q

Hyponatremia

A

develops with serum sodium concentration falls below 135 mEq/L. Loss of sodium, inadequate intake, dilution by water excess, vomiting, diarrhea.

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11
Q

S/S of hyponatremia

A

Excretion of water is impaired, decrease ability to depolarize and repolarize normally, altering action potential in neurons and muscle, lethargy, confusion, depressed reflexes, seizures, coma, muscle twitching, weakness

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12
Q

Hyperkalemia

A

(>5.5 mEq/L)

CAUSES: increase intake, shift of K from ICF into ECF, Decreased renal excretion, insulin deficiency, cell trauma

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13
Q

S/S of hyperkalemia

A

Renal Failure, loss of muscle tone/paralysis, decreased cardiac conduction and heart rate (bradycardia-cardiac arrest), increased neuromuscular irritability, tingling of lips/fingers, restlessness, intestinal cramping, diarrhea

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14
Q

Hypokalemia

A

(

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15
Q

S/S of hypokalemia

A

Skeletal weakness, cardiac dysrhythmias, impaired urinary contractibility, decrease in neuromuscular excitability, smooth muscle atony

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16
Q

Hypercalcemia

A

?

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17
Q

S/S of hypercalcemia

A

?

18
Q

Hypocalcemia

A

?

19
Q

S/S of hyopcalcemia

A

?

20
Q

Pyelonephritis

A

infection of one of both upper urinary tracts

can be acute or chronic (recurrance of acute version over and over)

21
Q

Acute Pyelonephritis

A 
S/S: 
onset of fever
flank and groin pain
frequency
dysuria
costovertebral pain (hand on back test)

Evaluation:
urinalysis
cultures (can take up to 72 hours)

22
Q

Chronic Pylonephritis

A 
S/S:
hypertension
frequency
dysuria
flank pain 
progression can lead to kidney failure

Evaluation:
profusion tests
ultrasound
urinalysis

23
Q

Causes of glomerulonephritis

A

immunologic abnormalities
drugs and toxins
vascular disorders
systemic diseases

24
Q

Changes in glomerular structure

A

Glomeruli THICKEN AND HARDEN

  1. Deposition of circulating soluble antigen-antibody complexes, often with complement fragments (Type III hypersensitivity);
  2. Antibodies reacting in situ against planted antigens within the glomerulus (Type II hypersensitivity–cytotoxic) or as she said in class: there’s an infiltration into the basement membrane and the complement becomes deposited, which attracts phagocytes, which then proliferate the inflammation;
  3. Nonimmune (drugs/toxins/ ischemia or as she said in class, blood flow decreases and there is lack of oxygen.
25
Q

Prerenal AKI causes

A

HYPOVOLEMIA, sudden and acute drop in blood flow in healthy, normal kidney, perhaps due to trauma (shock, hemorrhage, hypotension); ARF often caused by AKI (prerenal)

26
Q

Intrarenal AKI causes

A

ACUTE TUBULAR NECROSIS: problem inside kidney due to direct damage of inflammation, toxins, drugs, infections or reduced blood supply to kidney (a functional problem in kidney); ATN – most common cause or intrarenal failure; damage to kidney tissues and a structural change in tubular structure

27
Q

Postrenal AKI causes

A

OBSTRUCTIVE UROPATHIES (usually bilateral), caused by obstructions (stones, edema, tumors, strictures) that happen past the kidneys themselves (like in bladder or urethra)

28
Q

Patho of CKD

A

Progressive loss of renal function that affects nearly all organ systems. Associated with HTN, diabetes, intrinsic kidney disease

29
Q

S/S of CKD

A

proteinuria

uremia (due to glomerular hyperfiltration and damages interstitial tissue of kidney via inflammation)

creatinine and urea clearance (GFR falls and plasma creatinine increases)

hyponatremia - when we have CKD, kidneys can’t balance electrolytes…aka there’s not concentration/dilution control – therefore, due to bad Na/H2O balance,

hyperkalemia

dysrythmias

risk of hypocalcemia d/t decrease in vitamin D

lipidemia d/t LDL and Triglycerides rise and HDL lowers

metabolic acidosis is also a huge risk factor.

After GFR reaches 25% or below, patients are at risk for a whole lot of complications

30
Q

Evaluation of CKD

A

CARDIOVASCULAR – dyslipidemia due to build up of atherosclerosis, hypertension due to imbalance of Na/H2O, increased risk of heart failure, increased workload of heart due to anemia (ex. If we normally have 100 hemoglobin, with CKD we have only 50 and so the heart has to circulate those hemoglobin twice to get the same about of oxygen to the body as with the normal 100…hence increased heart work)

PULMONARY – complications due to fluid volume overload so body will dump that extra fluid into the lungs

HEMOTALOGIC – anemia, coagulations, platelets don’t function properly, there are alterations in thrombin, and increased tendency to bleed

IMMUNE – suppressed immune system, which causes abnormal reactions of immune system

NEUROLOGIC – headaches and pain, low Na, potential for seizures and coma activity, muscle twitching

GI – uremic gastroenteritis (inflammation), ulcers, hemorrhage, nausea, vomiting/diarrhea, anorexia, uremic factor (really bad breath because tons of waste leaving mouth)

ENDOCRINE AND REPRODUCTION – decrease in testosterone, infertility, decrease in libido, insulin resistence (and takes longer for kidneys to process meds when there’s CKD)

INTEGUMENTARY – pallor, bleeding into skin, increased bruising

31
Q

Leukemia - correlation between S/S and the cause

A

S/S/ Anemia CAUSE: decreased stem cell input or ineffective erythropoiesis or both

S/S Bleeding CAUSE: reduction in megakaryocytes leading to thrombocytopenia

S/S Infection CAUSE: opportunistic organisms, decreased protection (chemotherapy, corticosteroids, and disease process)

S/S Weight Loss CAUSE: pain, depression, chemo, radiation, loss of appetite, and alterations in taste

S/S Liver, Spleen, and lymph Node Enlargement: CAUSE: leukemic cell infiltration, lymph nodes also undergo leukemia proliferation in CLL

S/SElevated Uric Acid Level CAUSE: Increased catabolism of protein and nucleic acid; urate precipitation increased from dehydration caused by anorexia or fever and drug therapy

32
Q

Antigen

A

any substance capable of inducing a specific immune response and of reacting with the products of that response, i.e., with specific antibody or specifically sensitized T lymphocytes, or both.

33
Q

Antibody

A

an immunoglobulin molecule that reacts with a specific antigen that induced its synthesis and with similar molecules; classified according to mode of action as agglutinin, bacteriolysin, hemolysin, opsonin, or precipitin. Antibodies are synthesized by B lymphocytes that have been activated by the binding of an antigen to a cell-surface receptor.

34
Q

Type I : anaphylactic (IgE mediated)

A

MOST ALLERGIC REACTIONS

  • against environmental stimuli (allergens) → antigen reacts with IgE bound to mast cells → histamine released (edema, itching, hives)
  • food allergy may initiate an anaphylactic response and death
  • pruritus, edema, bronchospasm, dysrhythmias, increased blood flow (vasodilation), uticaria, GI cramping, hypotension, dizziness
35
Q

Type II: cytotoxic; IgG and IgM mediated

A

AGAINST SPECIFIC CELL OR TISSUE

  • cell is killed by antibodies and complement activation → phagocytosis → soluble antigen (foreign object) enters circulation and be deposited on tissues → antibody-dependent cell-mediated cytotoxicity (any substance that is toxic to cells) → causes malfunction
  • 1st time without reaction
  • Graves disease, hemolytic disease of Newborn (Rh incompatibility: Rh- mom and Rh+ fetus), Anemia
36
Q

Type III: Immune complex-mediated

A

AGAINST ANTIGEN FORMED IN BLOOD/BODY FLUID

  • IgG and IgM unites with antigen and form large complex which are deposited in vessel walls = neutrophils try to phagocytize cells but complement is too large
  • facial rash, serum sickness, Raynaud’s disease, lupus erythematous, oral ulcers, arthritis
37
Q

Type IV: Cell-mediated reaction

A

MEDIATED BY T LYMPHOCYTES

Mediated by T lymphocytes and do not involve antibody
-graft rejection, skin test for TB, poison ivy

38
Q

Clinical Manifestations of Cancer

A

PAIN: generally associated with late stages of cancer: in those terminally ill, anxious/afraid, lack of sleep, or fatigue
Caused by pressure, obstruction, and invasion of a structure sensitive to pain, stretching, tissue destruction, and inflammation.

FATIQUE: most frequently reported symptoms of cancer and treatment
Physiologic-decreased muscle contractility, sleep disturbances, decreased level of activity and nutritional status

CACHEXIA: anorexia, early satiety, weight loss, anemia, asthenia (marked weakness), taste alterations, and altered protein, lipid, and carb metabolism results in protein-calories malnutrition, and progressive wasting

ANEMIA: usually occurs because of malnutrition, chronic bleeding and resultant iron deficiency, chemotherapy, radiation, and malignancies in the blood-forming organs

LEUKOPENIA/THROMBOCYTOPENIA: decreased number of platelets
Caused by direct tumor invasion of bone marrow
Many chemotherapeutic drugs are toxic to bone marrow
Major cause of hemorrhage

INFECTION: Most significant cause of complications of death in persons with malignant disease; immunosuppression; granulocyte count falls below 500 cells

GI TRACT MANIFESTATIONS: Oral ulcers, malabsorption, and diarrhea, risk of infection d/t disruption of barrier → relies on rapidly growing cells to produce effective barrier to trauma and infection and absorption of nutrients

HAIR (alopecia) and skin: hair loss usually temporary, skin breakdown and dryness; erythema, alopecia (chemotherapy)

39
Q

Paraneoplastic syndromes

A

are rare system complexes, often caused by biologically active substances released from a tumor or by an immune response triggered by a tumor, that manifest as symptoms not directly caused by the local effects of cancer

Some paraneoplastic syndromes are: cushing syndrome, SIAH, hypercalcemia, hypoglycemia

40
Q

Avenues in which normal cells mutate and become oncogenic

A

o POINT MUTATION – small scale changes in DNA, alteration of just one or a few nucleaotide pairs; but this has profound effects on activity of proteins.
o CHROMOSOMAL TRANSLOCATION – large changes of chromosome structure and DNA; characterized by excess production of a proliferation factor; in these translocations large regions of DNA can be gained and lost – see steps:
1. Active oncogenes cause excess and inappropriate production of proliferation or growth factors
2. chromosome translocations then lead to production of novel proteins that promote growth
o COPY NUMBER VARIATION/AMPLIFICATION – can amplify oncogenes and delete tumor suppressor genes

Patho (8 decks)

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