Patho III Flashcards
Acidosis
Hypoventilation
(increased CO2 causes decreased pH)
Alkalosis
Hyperventilation
Hypercapnia
Too much CO2 in the blood.
Carcinoma
Cancer in Epithelial Tissue
Pulmonary Neoplasms
Right lung-more common, upper lobe, anterior
Listed most common to least common:
- Squamous Cell Carcinoma (curable)-centrally located in tree, slow growth, late metastisis-one year, non-productive cough (suspect pneumonia)
- Adenocarcinoma (glandular-not good)-arises in peripheral bronchial gland, invades lymphoid tissue and blood vessels before primary site is recognized.
- Large Cell Carcinoma-malignant cells are large, more peripheral in bronchial tree, rapid growth, proliferate and metastisize early.
- Small Cell (Oat Cell) Carcinoma-(worst to get)-very young cells, quick doubling time, metastisis. 5 year survival <5%. most die within 18 months.
Hematocrit
Volume percentage of RBC’s in blood
Should ALWAYS be 3X HgB
M=42-53%
F=38-46%
Aplastic Anemia
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”
Megaloblastic Anemia
Macrocytic-Normochromic
B12 and folic acid deficiency
RBC’s produced are big and flimsy-shorter life span
blastic=young
(eg. pernicious anemia)
Iron Deficiency Anemia
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)
Sickle Cell Anemia
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
Other Hemoglobinopathies
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.
Polycythemia
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
MCV
MCHC
MCH
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
WBC’s
4,000 -10,000 /mm3
composition of WBC’s tells us more
WBC’s do have nucleus
Granulocytes
granuoles kill engulfed bacteria with “bleach” and H2O2
If pt has 85%=bacterial infection
PMN (=polymorphic neutrophils/segmented neutrophils/SEGS)
Stab (BAND)
Eosinophils
Basophils
Stab (BANDs)
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
PMN (SEGS)
38-70% of all WBCs
should be segmented (nucleus is segmented)
most intimately involved in phagocytizing bacteria
elevated SEGS = bacterial infection
Eosinophils
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
Basophils
0-2% of WBC’s
don’t know much ab these
granuoles produce histamine
Non-Granulocytes
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)
Leukocytosis
WBC’s higher than 10,000 mm3
opposite=leukopenia
Granulocytosis
Increase in granulocytes-normally refers to SEGs since they are most numerous
Neutrophilia
Increase in SEGs
most common reason-bacterial infection
Toxic Granulation
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
Left Shift
Increase in # of SEGs, bands
Right Shift
Increase in number of lymphocytes, monocytes
Leukopenia
decrease in total number of WBCs (below 4,000)
opposite=leukocytosis
Agranulocytosis
=absence of SEGs
also expect leukopenia with this since SEGs are mose prevelant granulocyte
A BAND is to a SEG
As a reticulocyte is to a RBC
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
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
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
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
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
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
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
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
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
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
Serotonin
Vasoconstrictor
Coagulation
- intrinsic-(longer-5-10 min-8,9,11,12); extrinsic-(10s-factor 7) *PROTHROMBINASE aka thromboplastin
- Prothrombin→Thrombin (initiated by prothrombinase)
- Fribinogen→Fibrin (initiated by thrombin)
Stages 2 and 3 are intrinsic
…………………………………………………………………………..
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
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
Acquired Factor Deficiency
(ie. not hereditary)
2 ways to get here:
- Decreased production (not producing enough coagulation factors) liver disease, vit K deficiency
- Increased consumption (consuming too much of coagulation factor)
Liver Synthesis of coagulation factors
2,5,7,9,10
liver pathology=not enough of these factors
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
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
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
Plasmin
Fibrinolytic
Circulates in plasma as plasminogen (must be activated)
Produced by megakaryocytes in bone marrow-detachment of cytoplasmic filaments
Acute Superficial Gastritis
inflammation of gastric mucosal lining
(stomach ache)
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.
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
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)
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
Bilirubin
conjugated=glucuronic acid-takes place in liver=direct
unconjugated=attached to albumin, water insoluble=indirect
- increased production (red cell breakdown)
- impairment of hepatic uptake (side effect of meds, some dyes)
- impairment of conjugation of bilrubin (lack of enzymes–infants, Gilbert’s Syndrome)
- decrease in liver’s ability to excrete (pathology)
