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Patho III > Patho III > Flashcards

Patho III Flashcards

1
Q

Acidosis

A

Hypoventilation

(increased CO2 causes decreased pH)

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2
Q

Alkalosis

A

Hyperventilation

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3
Q

Hypercapnia

A

Too much CO2 in the blood.

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4
Q

Carcinoma

A

Cancer in Epithelial Tissue

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5
Q

Pulmonary Neoplasms

A

Right lung-more common, upper lobe, anterior

Listed most common to least common:

  1. Squamous Cell Carcinoma (curable)-centrally located in tree, slow growth, late metastisis-one year, non-productive cough (suspect pneumonia)
  2. Adenocarcinoma (glandular-not good)-arises in peripheral bronchial gland, invades lymphoid tissue and blood vessels before primary site is recognized.
  3. Large Cell Carcinoma-malignant cells are large, more peripheral in bronchial tree, rapid growth, proliferate and metastisize early.
  4. Small Cell (Oat Cell) Carcinoma-(worst to get)-very young cells, quick doubling time, metastisis. 5 year survival <5%. most die within 18 months.
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6
Q

Hematocrit

A

Volume percentage of RBC’s in blood

Should ALWAYS be 3X HgB

M=42-53%

F=38-46%

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7
Q

Aplastic Anemia

A

normocytic, normochromic

production problem-bone marrow is shut down-not producing any formed elements (RBC, WBC, platelets or bone tissue)

(anemic, infected, bleed)

Dystrophic-putting fatty tissue in the bone instead of bone tissue. Bones become soft, break.

Causes: medications, radiation of bone marrow, mustard gas (WWI)

“Pancytopenia”

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8
Q

Megaloblastic Anemia

A

Macrocytic-Normochromic

B12 and folic acid deficiency

RBC’s produced are big and flimsy-shorter life span

blastic=young

(eg. pernicious anemia)

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9
Q

Iron Deficiency Anemia

A

Microcytic-hypochromic

HbB=7 Hematocrit=21

chew on ice, tired/fatigue, broken nails smooth, pale, white tongue, split ends, frizzy

Could be diet or absorption, could be protein Fe is carried on (transferrin)

too much iron=toxic (pathogens hold on to your Fe)

=chronic blood loss (eg. slow dripping ulcer)

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10
Q

Sickle Cell Anemia

A

Hemoglobinopathy (35 of these-all genetic)

HgB=2 alpha, 2 beta protiens-2 aa’s change places (valine and glutamic acid)=HgB-S (instead of HgB-A)

Low O2-HgB crystallizes and cell sickles-gets clogged in capillaries

Problem at joints bc low O2 there

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11
Q

Other Hemoglobinopathies

A

Hemoglobin C disase (2 different aa’s switch places)

Hemoglobin S-C disease (sickle cell AND amino acid switch of HgB C disease)

Newborns make HgB-F (fetal)–not a pathology–enormous affinity for O2-for first 3-4 months, then becomes more like adult.

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12
Q

Polycythemia

A

Too many RBC’s

“relative” HgB 15, Hematocrit 68%, RBC count 4.5 pt is dehydrated (not true polycythemia)

“absolute” RBC: 8.5, HgB 22, Hematocrit 67%, elevated BP, losing lots of RBC’s, not enough protein to take care of Fe release-lots of free Fe, blood is thick, viscous, thrombosis=BLEED them; extra free Fe ends up in liver and is toxic=damage=death

“reactive” physiological polycythemia-heavy smokers (3+ packs/day) Kidneys aren’t getting perfused-erythropoitin-more RBC’s to make up for those carrying CO

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13
Q

MCV

MCHC

MCH

A

Used when trying to determine why an anemia is occuring.

mean corpusclular volume (81-96 mm3)

mean corpusclular HgB concentration (HgB=30-36g/100 mL)

mean corpuscular HgB

these are calculated from HgB, RBC, HCT

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14
Q

WBC’s

A

4,000 -10,000 /mm3

composition of WBC’s tells us more

WBC’s do have nucleus

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15
Q

Granulocytes

A

granuoles kill engulfed bacteria with “bleach” and H2O2

If pt has 85%=bacterial infection

PMN (=polymorphic neutrophils/segmented neutrophils/SEGS)

Stab (BAND)

Eosinophils

Basophils

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16
Q

Stab (BANDs)

A

1-2% of WBC’s

c shaped nucleus

immature, adolescent neutrophil

can’t phagocytize as well as a SEG

Increase in SEGs prob = increase in BANDs

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17
Q

PMN (SEGS)

A

38-70% of all WBCs

should be segmented (nucleus is segmented)

most intimately involved in phagocytizing bacteria

elevated SEGS = bacterial infection

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18
Q

Eosinophils

A

1-5% of WBCs

segmented nucleus

big orange granules in cytoplasm

don’t do a lot

increases: parasitic infections, allergic reactions-produce histamine, have exact receptor site for IgE-allergen stimulates these cells to release histamine

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19
Q

Basophils

A

0-2% of WBC’s

don’t know much ab these

granuoles produce histamine

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20
Q

Non-Granulocytes

A

Lymphocytes-great big nucleus

15-45% of all WBC’s-antibody production, if elevated = viral infection (lymphocytosis)

Monocytes-big cells, big nucleus

1-8% of all WBC’s

ability to transform into macrophages=clean up crew after infection=recuperative phase

(monocytosis=increase in monocytes)

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21
Q

Leukocytosis

A

WBC’s higher than 10,000 mm3

opposite=leukopenia

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22
Q

Granulocytosis

A

Increase in granulocytes-normally refers to SEGs since they are most numerous

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23
Q

Neutrophilia

A

Increase in SEGs

most common reason-bacterial infection

24
Q

Toxic Granulation

A

granulation is bigger, more intense, more of them

granuoles phagocytize bacteria=bigger, meaner infection that has been going on for a few days. it takes bone marrow a few days to produce these cells

25
Q

Left Shift

A

Increase in # of SEGs, bands

26
Q

Right Shift

A

Increase in number of lymphocytes, monocytes

27
Q

Leukopenia

A

decrease in total number of WBCs (below 4,000)

opposite=leukocytosis

28
Q

Agranulocytosis

A

=absence of SEGs

also expect leukopenia with this since SEGs are mose prevelant granulocyte

29
Q

A BAND is to a SEG

A

As a reticulocyte is to a RBC

30
Q

Leukemia

A

Acute vs. Chronic

Cell Line

Hallmark: anemic, bleed, infected

All are diagnosed bone marrow biopsy

Liver/spleen enlarged=recycling all of the blood cells

31
Q

Acute Myeloctytic Leukemia

A

cells go through 2 developments (stem cell-pro myeloctye-myelocyte-formed element) before commiting to specific granulocyte.

this leukemia begins from the myelocyte-immature cell

80% younger adults (20-40s)

more common in males

less than 20% live 5 years

presents: pt is fatigued, flu-like, weight loss, bruising (petechia)

WBC count=200,000!!!

no RBCs, no WBCs, no platelets being produced

anemic, infected, bleeding

live 3-6 months

90% have abn gene on chromosomes 5,7,11,16 or combo.

Treat with chemo-targeting rapidly reproducing cells

32
Q

Acute Lymphocytic Leukemia

A

80% are children (age 3-4)

more common male

pt presents: not acting right, no energy, no appetite, bruises (petechiae), WBCs - 80,000 to 100,000, enlarged liver, spleen

Good prognosis-95% permanent remission

other 5% responds to bone marrow transplant

33
Q

Chronic Granulocytic Leukemia

A

=middle aged leukemia, insidious,slow

WBC = 30,000 (initially 12,000-suspect infection)

85% have abnormal gene #22 (Philadelphia chromosome)

diagnose-biopsy bone marrow

34
Q

Chronic Lymphatic Leukemia

A

=Old people (age 60-male)

50% abnormal gene chromosome #12

pt has abdominal complaints=bowel disturbances

WBC = 12,000, then 13,000, then 14,000

takes time to diagnose

GI problems from enlarged liver pressing on GI-palpate

Often-pre-existing disease, cancer complicates

35
Q

Lymphoma

A

Epstein-Barr Virus

Hodgkins-age 18-35, more male than female; typical pt: swelling in neck, armpit, groin for 1 month, no pain, but hard and rubbery, 25% also have night sweats

Non-Hodgkins-50 yrs, 8-10 yr survival, night sweats and enlarged nodes; pt succumbs to pre-existing disease

Diagnose: biopsy lymph node

36
Q

Lymphoma Stages

A

Stage 1 = 1 node

Stage 2 = 2+ adjacent/2+ non-adjacent on same side of diaphragm

Stage 3 = nodes above and below diaphram

Stage 4 = metastisis to other organs

Sutton’s Law–go for biggest lymph node

37
Q

Multiple Myeloma

A

proliferative disorder associated with plasma cells in marrow instead of RBC’s, platelets, WBC’s and bone

median age = 60, male

Plasma cells ultimately produce antibodies-B-lymphocytes…weird anitbodies

Pancytopenia!!!

Treat like you treat leukemia-drugs that decrease excessive proliferation of plasma cells

38
Q

Waldenstrom’s Macroglobulinemia

A

Rare, proliferative

mostly males, middle age

can look like multiple myeloma

extreme over production of IgM antibodies

IgM’s are temp sensitive=extreme Raynaud’s

So much IgM=viscous blood=increase in BP, pressure on brain

39
Q

Thrombocytosis

Thrombocytopenia

A

increase in PLATELETS (>400,000 mm3)

decrease in PLATELETS (<100,000 mm3)–no bleeding until below 50,000

Rule of thumb=petechiae <30,000

<20,000 = risk of spontaneous intracranial bleed

40
Q

Serotonin

A

Vasoconstrictor

41
Q

Coagulation

A
  1. intrinsic-(longer-5-10 min-8,9,11,12); extrinsic-(10s-factor 7) *PROTHROMBINASE aka thromboplastin
  2. Prothrombin→Thrombin (initiated by prothrombinase)
  3. Fribinogen→Fibrin (initiated by thrombin)

Stages 2 and 3 are intrinsic

42
Q

…………………………………………………………………………..

Genetically Inherited Plasma Factor Deficiency

(recessive, X-linked)

A

Hemophilia A=deficient factor 8 (most common)

Hemophilia B (Christmas Disease)=deficient factor 9

(NOTE: both are from stage 1, both are intrinsic)

PTT (intrinsic) = abnormal

PT (extrinsic) = normal

Both=normal bleeding time, but Fibrin isn’t formed

VonWildenbrands Disease (Hemo A/B AND platelets are lacking) = BLEEDING AND COAGULATION PROBLEM

43
Q

Coagulation Tests

A

PTT (partial thromboplastin time)=problems stem from intrinsic side of stage 1, and problems in stages 2 and 3

PT (prothrombin time)=problems with extrinsic side of stage 1 and problems with stage 2

44
Q

Acquired Factor Deficiency

(ie. not hereditary)

A

2 ways to get here:

  1. Decreased production (not producing enough coagulation factors) liver disease, vit K deficiency
  2. Increased consumption (consuming too much of coagulation factor)
45
Q

Liver Synthesis of coagulation factors

A

2,5,7,9,10

liver pathology=not enough of these factors

46
Q

Vitamin K

A

Required to activate factors 2,7,9,10

If pt has an MI, put them on blood thinner (anti-coagulant) like Coumadin (rat poison)–decreases the level of vitamin K–not an immediate effect–indirect approach

Heparin (produced in liver)=immediate effect bc it interferes with 2nd step of coagulation

47
Q

DIC

(Disseminating Intravascular Coagulation)

A

Acquired factor deficiency=increased factor consumption

mostly OB pts-due to premature placental detachment; placenta is rich source of thromboplastin (aka prothrominase) which leaks into the vascular system=contiual clot formation/clot breakdown); after delivery-she can’t clot bc factors are gone.

Also occurs in trauma-massive bacterial exotoxins-some bacterial exotoxins are interpreted by the body as prothrombinase–which causes body to form clots which causes the activation of fibrinolysis; major complication=breakdown of clots needed for injury–give pt heparin

48
Q

STROKE

A

Give TPA for clot (tissue plasminogen activator)–converts plasminongen (circulating in blood) into plasmin

Plasmin is fibrolytic (breaks down fibrin=canalization)

CT scan to determine if stroke is a clot or a bleed

49
Q

Plasmin

A

Fibrinolytic

Circulates in plasma as plasminogen (must be activated)

Produced by megakaryocytes in bone marrow-detachment of cytoplasmic filaments

50
Q

Acute Superficial Gastritis

A

inflammation of gastric mucosal lining

(stomach ache)

51
Q

Chronic Atrophic Gastritis

A

gradual atrophy of the glandular epithelial tissue

decrease in chief cells-loss of HCl, pepsin production, intrinsic factor (pernicious anemia), predisposed to gastric ulcers and stomach cancer.

52
Q

Crohn’s Disease

A

=regional enteritis

chronic inflammatory disease-80% in terminal ileum

skip lesions-areas of inflammation-lymph nodes

mycobacterium ? (not same sp as TB)/autoimmune

runs in families-have to have parts of ileum removed

53
Q

Ulcerative Colitis

A

young (20-40), type A

Acute fulminating-acute onset (10% die)-poor prognosis

Chronic Intermittent 70%

Chronic contiunuous-spicy foods, nuts may excasterbate

Complications: megacolon (transverse colon shuts down)–can rupture (30% mortalitiy)

54
Q

Polyps

A

growths arising from mucosal lining of GI tract

Polypoid adenomas-7-10% of pop over 45…not correlated with any pathology

Villous adenoma–sigmoid colon and rectum, larger, 25% become malignant

Familial polyposis-rare, dominant gene, 100% malignant by 40

55
Q

Bilirubin

A

conjugated=glucuronic acid-takes place in liver=direct

unconjugated=attached to albumin, water insoluble=indirect

  1. increased production (red cell breakdown)
  2. impairment of hepatic uptake (side effect of meds, some dyes)
  3. impairment of conjugation of bilrubin (lack of enzymes–infants, Gilbert’s Syndrome)
  4. decrease in liver’s ability to excrete (pathology)

Patho III (3 decks)

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