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Patho Exam #2 > Pink Pigs > Flashcards

Pink Pigs Flashcards

0
Q

What is cytotoxic T cells?

A

T cells that attach to mhc-1 and kills the cells that infected. Once it activated, it divide it memory cell, and effector cells which kills any cells that has turn abnormal, etc cancer cells

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1
Q

What is clonal selection?

A

Cells makes a lot of B cells which can only creat a certain type of antibodies. Stimulation of only the B cells that react to the antigen is referred to clonal selection. Once B cells activated, it divide rapidly producing B cells clones. B cells then differentiate to plasma cells and memory cells. Plasma cells makes antibodies

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2
Q

What is antibody?

A

Known as immunegobulin (Ig) kills specific antibodies

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3
Q

What is Ig E?

A

Make immediate response, can be local or systemic. Allergen activates it which bind to mast cell which produce histamine( triggers complement system)

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4
Q

What the treatment for activating Ig E?

A

Epinephrine, antihistamine, corricosteriod

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5
Q

What the clinical manifestation of activating Ig E?

A

Like allergic reaction, redness, swelling warmth at site, etc

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6
Q

What is type 2 :tissue specific hypersensitivity?

A

Ig G or IgM, reacts to foreign tissue cells. Antibodies bind on the cell surface and destroy or prevent cells from functioning. Usually quick response

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7
Q

What is type 3 hypersensitivity?

A

Immune complex mediated, triggers the complement system and inflammation; attracting basophils which release emzymes that destroys tissues
Mostly cause by antigen antibody complexes

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8
Q

What is type 4 hypersensitivity?

A

It’s cell mediated hypersensitivity specifically by T lymphocytes. Ex graft rejection,or TB skin testing. 24 to 72 hrs until it initiated, slow onset

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9
Q

What is Ig G?

A

Most abundant class, 85% of Ig in blood that most protective activity against infections. It the most abundant in baby’s and fetus as well

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10
Q

What is Ig A?

A

2 subclass: IgA1 and IgA2. IgA1 is found mostly in blood, IgA2 is found mainly in body secretion.

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11
Q

IgM

A

Largest Ig, first antibody produce during the initial or primary response to antigen. Synthesize early in neonatal life

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12
Q

IgD

A

Low concentration in the blood. It’s primary function is a antigen receptor on the surface of early B cells

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13
Q

What is B cells?

A

When B cells gets activated ; binding of antigen and stimulation if helper T cells by binding to MHC 2. Once activated B cells, it start to divide and differentiated to memory cells and plasma cells. Plasma cells tags to the antigen which can get recognize to macrophages

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14
Q

What is T cells?

A

Nk killer cells, 2 type with either CD4 and CD 8 T cells. CD4 T cells are the one that want to bind to MHC II which is mostly T helper cells. CD. 8 binds to MHC 1 complex which kills bad cells, eg cancer cells. Once activated, it start to divide and differentiate to effector cells and memory cells. The effector helper T cells can activate B cell and release cytokines. Cytokines mainly help be the alarm ringer for everyone to get ready

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15
Q

What is the CD4 T cells?

A

“General” sends signals to activate immune response when there is intruder. HIV infects it and take over the immune cells

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16
Q

What is alpha adrenergic receptors?

A

A1 receptors: eyes dilate, blood vessels will vasoconstrict which increase Bp. It also increase spincter tone which decrease urine output.
A2 receptor decrease insulin production.

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17
Q

What is beta adrenergic receptor?

A

Beta 1: increase conduction and HR and cardiac output. Beta2; bronchodilator, dilate blood vessels

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18
Q

What is rheumatoid arthritis?

A

Autoimmune disease, 3:1 female: male. Onset 40-60 years old. It systemic, inflammatory response. Bilateral joint pain and swelling. The synovial membrane is the first to be affected. Degeneration and lost of the articulate cartilage, the inflame cells can go in the heart and spleen.

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19
Q

What the patho of RA?

A

Neutrophils in synovial fluid are activated. Articular cartilage becomes degraded.

20
Q

What the clinical manifestation of rheumatoid arthritis?

A

Begins as acute inflammatory episode that appear to recover: generalize manifestation, fever, weakness, weight loss, generalize aching and stiffness. Morning stiffness lasting more than 1 hr. Joint swelling is wide spread and symmetric, joints warm to touch

21
Q

What the diagnosis of RA?

A

Serum rheumatoid test— high
Erythrocytes sedimentation test - test inflammation in your body but does not tell location
Synovial fluid analysis
Joint x-Ray MRI

22
Q

What the treatment of RA?

A

No cure, early aggressive treatment can slow joint destruction, pain management and promoting independence

23
Q

What the pharmacological approach toward RA?

A

Nonsteriodal antiinflammatory drugs, corticosteroid– moon face and mood changes
Disease modifying antirheumatic drugs , methotrexate- help decrease immune response. Anti- malarial drugs
TNF- Inhibitor (Remicade, Humira,Enbrel) help stop debriding of tissue

24
Q

What is AIDS?

A

HIV Parasitic retrovirus that infects and destroys the helper T cells. Type 1: common strain, type 2: more common in west Africa, disease progress more slowly. Transmit through blood and bodily fluids

25
Q

What is catecholamines

A

Adrenal medulla, epinephrine, norepinephrine( adrenaline)-

26
Q

What is hydrostatic pressure?

A

Pressure within the fluid that at rest, remain equal. The pressure that pushing outward of the capillaries. The osmotic pressure the pressure that going toward the capillaries

27
Q

What is oncotic pressure?

A

Water follows wherever there higher osmolarity. Oncotic pressure is similar to oncotic pressure but it mainly protein, most abundant protein is albumin which is made in the liver. Higher oncotic pressure equal higher water

28
Q

What is antidiuretic hormones?

A

Increases Bp, vasoconstriction, retain water increasing the blood volume and larger stroke volume

29
Q

What is hypertonic iv solution and how does it relate to the cells?

A

3% NaCl, D5 .45% a And .9% NS, 10% Dextrose

30
Q

What is aldosterone?

A

The RAAS club, aldosterone retain Na which increase water volume

31
Q

Respiratory acidosis

A

Low ph and high co2
Risk factor copd, narcotics
S/sx- hypoventilation, blurred vision, confusion

32
Q

Respiratory alkalosis

A

High ph low co2
Risk factor: anxiety, hyperventilating, fever, mechanical ventilation
S/sx hyperventilating, numbness and tingling at mouth , chest tightness, palpitation

33
Q

What the normal body ph?

A

7.35-7.45

34
Q

Normal paco2

A

Normal PaCO2 35-45

35
Q

Normal PaO2

A

80-100

36
Q

Normal HCO3

A

22-26

37
Q

What is metabolic acidosis?

A

Low ph low hco3
Risk factor, DKA, renal failure, diarrhea, intestinal auctioning
S/sx anorexia, warm flush skin. decrease LOC

38
Q

Metabolic alkalosis

A

High ph and high hco3
Risk factor: extensive use of diuretics, gastric auctioning. Vomiting,diuretic therapy
S/sx respiratory failure, dysthymia , altered LOC

39
Q

What the normal anion gap?

A

8-12 mEq/L

40
Q

What is acute renal failure?

A

When the kidney lost their function?

41
Q

What the cause of acute renal failure?

A

3 causes , prerenal-lack of blood flow to the kidneys, post renal- obstruction of the kidney, intrarenal: damage to the nephrons itself

42
Q

Renal function??

A

Urea (BUN)goes up

Creatinine clearance

43
Q

What is prerenal failure?

A

Decreased blood flow, 55% of ARF. Reversible or can progress to intrarenal failure

44
Q

What is intrarenal failure?

A

Damage to the tissue and nephrons

Acute tubular necrosis: ischemia is the most conmon cause, rhabdomyolysis, nephrotoxic drugs, glomerulophritis,

45
Q

What is post renal failure?

A

Obstruction of the kidneys . BPH, urinalysis calculi, tumors

46
Q

What the 3 phases of renal failure?

A

Initiating phase- ends when tubular injury occurs
Maintainence phase- oliguric, diuretic period
Recovery phase

47
Q

What is oliguric phase?

A

Cannot eliminate waste, water, and electrolytes

Patho Exam #2 (5 decks)

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