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Patho III Flashcards

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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

Study These Flashcards
A

Increase in SEGs

most common reason-bacterial infection

24
Q

Toxic Granulation

Study These Flashcards
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
Left Shift
Increase in # of SEGs, bands
26
Right Shift
Increase in number of lymphocytes, monocytes
27
Leukopenia
decrease in total number of WBCs (below 4,000) opposite=leukocytosis
28
Agranulocytosis
=absence of SEGs also expect leukopenia with this since SEGs are mose prevelant granulocyte
29
A BAND is to a SEG
As a reticulocyte is to a RBC
30
Leukemia
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
Acute Myeloctytic Leukemia
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
Acute Lymphocytic Leukemia
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
Chronic Granulocytic Leukemia
=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
Chronic Lymphatic Leukemia
=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
Lymphoma
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
Lymphoma Stages
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
Multiple Myeloma
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
Waldenstrom's Macroglobulinemia
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
Thrombocytosis Thrombocytopenia
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
Serotonin
Vasoconstrictor
41
Coagulation
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
...................................................................................... Genetically Inherited Plasma Factor Deficiency (recessive, X-linked)
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
Coagulation Tests
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
Acquired Factor Deficiency (ie. not hereditary)
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
Liver Synthesis of coagulation factors
2,**5**,7,9,10 liver pathology=not enough of these factors
46
Vitamin K
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
DIC (Disseminating Intravascular Coagulation)
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
STROKE
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
Plasmin
Fibrinolytic Circulates in plasma as plasminogen (must be activated) Produced by megakaryocytes in bone marrow-detachment of cytoplasmic filaments
50
Acute Superficial Gastritis
inflammation of gastric mucosal lining (stomach ache)
51
Chronic Atrophic Gastritis
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
Crohn's Disease
=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
Ulcerative Colitis
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
Polyps
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
Bilirubin
**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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