Pathology Exam 2 Dr. Mcconnell

Front 1

What is the lifecycle and lifespan of RBC's and platelets?

Back 1

Blood cells are produced in the bone marrow, circulate for a number of days, and are removed, mainly by the spleen

RBC- have lifespan of 120 days

neutrophils, basophils, eosinophils - lifespan 4 days

lymphocytes & monocytes - 1-2 weeks
platelets - day or so

Front 2

explain what is meant by red cell indices, and understand how to calculate them

Back 2

-red cell indices are measures of red cell size & hemoglobin content
-they are calculated ratios among red cell count, hemoglobin, & hematocrit

Front 3

define Anemia:
& list the major types of anemia:

Back 3

-anemia is:
-- lower than normal blood hemoglobin or...
--lower than hematocrit levels or
--lower than normal red cell counts
Anemia causes: 1 decreased production of red cells, 2increased destruction of red cells, 3 loss of red cells (hemorrhage)

Front 4

Explain sickle cell anemia 's cause, and discuss what happens to red cells

Back 4

Sickle cell anemia occurs when there is a genetic defect in hemoglobin formation.
-the altered Hgb causes red cells to be deformed into a sickle (crescent) shape. Malformed RBCs clog capillaries and impair blood flow. -are prematurely destroyed/removed from circulation after less than 120 days

Front 5

explain blood & bone marrow ferritin, iron, transferrin, and iron binding capacity in iron deficiency anemia:

Back 5

Blood iron and ferritin and marrow ferritin are low because body iron stores are depleted.
-blood iron binding capacity is increased as a reflection of increased blood transferrin, a protein made by the liver, which is increased in order to attempt to transport more iron to tissues

Front 6

what is the difference between relative and absolute erythrocytotis?

Back 6

Relative erythrocytosis is: increased peripheral red cell count that is not associated with increased total body cell mass.
Absolute erythrocytosis is: associated with increased total body red cell mass

Front 7

Explain the significance of a left shit in the white cell differential count in peripheral blood

Back 7

A "left shift" is caused by release of immature granulocytes from bone marrow into peripheral blood. It occurs most often when the marrow is under stress, as when responding to acute infection.

Front 8

what are the 2 major groups of bone marrow malignancies?

Back 8

2 major groups:
-myeloid and lymphoid

Front 9

what are the major diseases associated with myeloid neoplasms?

Back 9

-are a varied group, consist of acute and chronic myeloid leukemia, and a family of related malignancies known as th
CHRONIC myeloproliferative syndromes

Front 10

what are the major diseases associated with lymphoid neoplasms?

Back 10

-acute and chronic lymphocytic leukemia, lymphomas, and plasma cell proliferations

Front 11

distinguish between Leukemia and Lymphoma

Back 11

-both are malginancies of leukocytes
-in leukemia: malignant cells are present throughout the bone marrow & are found in high numbers in peripheral blood

-in lymphoma malignant cells occur as nodular masses in lymph nodes and other organs, the bone marrow and blood are not much involved

Front 12

why do patients with plasma cell proliferation have abnormal blood proteins?

Back 12

plasma cell proliferations include:
benign & malignant growths of plasma cells that produce an excess of immunoglobulin

Front 13

name the 2 major types of lymphoma

Back 13

-Hodgkin lymphoma
-non-Hodgkin lymphoma

Front 14

what are the 2 types of non-Hodgkin lymphomas according to: -microscopic patterns, and explain why this distinction is important.

Back 14

2 types are follicular and diffuse.
-distinction is important because they behave much differently.
--follicular lymphomas are less aggressive & have better prognosis than diffuse ones.

Front 15

define: hypersplenism

Back 15

overactivity of the spleen that consumes more than the normal amount of WBC, RBC or platelets.
-hypersplenism is associated with enlarged spleen

Front 16

name the elements of normal hemostasis

Back 16

hemostasis depends upon the interplay of:
1- coagulation
2-blood vessel factors
3- platelets

Front 17

characterize bleeding caused by platelet disease

Back 17

bleeding is usually the result of low platelet count;
bleeding because of platelet malfunction is uncommon.
-the bleeding is usually from small, capillary size-blood vessels & appears as petechiae or other small hemorrhages

Front 18

briefly characterize classic hemophilia (or hemophilia A)

Back 18

it is an X-linked genetic deficiency of coagulation factor VIII that occurs in males;
mild deficiencies may cause excess post-traumatic bleeding;
-severe deficiency may cause spontaneous bleeding, esp. in joints.

Front 19

explain why patients with disseminated intravascular coagulation have bleeding problems

Back 19

--disseminated intravascular coagulation consumes clotting proteins (factors) leaving insufficient clotting proteins to support normal clotting.
the result is a tendancy toward hemorrhage.

Front 20

what are 2 steps in the diagnosis of anemia:?

Back 20

1-complete blood count & determination of red cell indices
2- determine if the anemia is associated with blood loss,red cell destruction, or failed bone marrow production of red cells

Front 21

hemorrhagic anemia

Back 21

-most common cause of Fe def anemia.
-chronic blood loss occurs with:
-abnormal menstrual bleeding in women, & intestinal bleeding in either sex, esp from undetced colon CA

Front 22

what is dilutional anemia?

Back 22

-features healthy red cells, which have normal size and Hgb content,

Front 23

hemolytic anemia is associated with?

Back 23

-active hypercellular bone marrow
-blood that contains a high count of new RBC
-increased blood lactic dehydrogenase
-low blood haptoglobin (protein that is freed from dead RBC & carries them away for disposal)
-increased blood bilirubin

Front 24

Other hemolytic diseases caused by genetic defect

Back 24

G6PD deficiency: x-linked, causes deficiency of G6PD in red cells. high in AA men.

Sickle celle disease:
Thalassemia: decreased Hgb production.

Front 25

thalassemia; type of cells it has & other fact

Back 25

-microcytic hypochromic anemia
(small pale red cells)
-due/to ineffective production: stimulates iron absorption from GI--> leads to iron overload (hemochromatosis)

Front 26

non genetic hemolytic anemia:
-immune hemolytic anemia

Back 26

caused by antibodies directed against antigens on RBCs
-assoc with autoimmune disease

Front 27

non genetic hemolytic anemia:
mechanical hemolytic anemia

Back 27

Mechanical hemolytic anemia: caused by physical shredding of red cells as they pass thru mechanical devices like artificial heart valves. (or when they squeeze thru inflamed blood vessels)

Front 28

non genetic hemolytic anemia:
malaria

Back 28

-parasites infect & destroy red cells, causing hemolysis, fever & jaundice occuring q 48-72 hours as new generations of parasites are produced.

Front 29

anemia of insufficient production:
-inadequate bone marrow RBC production

Back 29

-caused by deficiencies in B12, folate, iron.
-destruction or replacement of marrow leaving scar behind can lead to low RBC production

Front 30

iron deficeency anemia

Back 30

-microcytic hypochromic
-most attributed to blood loss,
-in fe deficiency:
-plasma transferrin (TIBC) is high
-plasma iron is low
-% sat of transferrin by Fe is low
MOST COMMON NUTRIENT DEFICIENCY

Front 31

B12 & Folic acid anemia

Back 31

macrocytic/megaloblastic anemia
-inadequdate diet or absorption
-B12 anemia- pernicious anemia
(autoimmune disease w autoantibodies against gastric mucosa & IF)

Front 32

anemia of chronic disease

Back 32

-low output of RBC by bone marrow
-diseases involved are usually cancer, chronic infections, chronic autoimmune disorders
-may look like Fe defcny anemia: BUT---> Fe def have small page red cells.
>pts with chronic disease anemia have abn or high plasma ferritin (fe stores plentiful)

Front 33

aplastic anemia (primary bone marrow failure)

Back 33

-it is a primary failure of ALL marrow elements (RBCs, WC, megakaryoctyes). low platelet count.
-anemia usually presenting problem. in fatal cases: hemorrhage cause of death.
-cause unknown, chemical agents usually responsible.

Front 34

myelophthisis
(anemia caused by bone marrow replacement/destruction)

Back 34

-when bone marrow is replaced by malignancy/fibrosis
-some cancers can do this (by crowding out blood making components)

Front 35

polycythemia
(too many red cells)

Back 35

-->excess no. of RBC in blood
-most common cause: low plasma volume (ex: dehydration).
--absolute: actual increase in total RBCs (occurs w/ marrow malignancy like myeloid leukemia)
--2ndary: caused by conditions outside marrow (hypoxia, high altitudes)

Front 36

Leukopenia

Back 36

low white blood cell count (caused by decr. of granulocyte numbers, esp neutropenia)
-caused by: failing bone marrow, by drugs/toxins or if marrow is replaced by neoplasm
--severe neutropenia = agranulocytosis

Front 37

leukocytosis

Back 37

-increase in WBC in peripheral blood
-benign --> (reactive)
-malignant --> malignant (leukemia)

Front 38

leukemia

Back 38

a malignant proliferation of white cells, either
-lymphoid cells (lymphocytes)
or
-myeloid cells (granulocytes or monocytes)

Front 39

lymphoma

Back 39

a malignant neoplasm of lymphocytes in lymph nodes and organs as nodular masses
-however lymphoma no malignant cells are detectable in blood

Front 40

lymphocytic leukemia

Back 40

leukemia of cells in the lymphoid line

Front 41

myelocytic leukemia

Back 41

leukemia of the cells in the myeloid line

Front 42

chronic leukemia

Back 42

-less aggressive, and runs a short course
-pts present with fatigue,pallor (from anemia)
-clinical course less rocky, better prognosis
-cause of death --hemorrhage as result of low platelet count (same as acute)

Front 43

acute leukemia is characterized by

Back 43

-abrupt onset, which often presents as an acute infection or hemorrhage
-symptoms related to a decrease in the numbers of normal marrow cells, such as might be seen in anemia, infection, or bleeding (from thrombocytopenia)
-bone pain & tenderness when bone marrow becomes packed w/ cells
-enlarged lymph nodes, spleen, liver, because of accumulations of malignant cells
-nervous system symptoms: HA, vomiting, nerve palsies from malignant cells infiltrating the meninges
-peripheral WBC counts are high

Front 44

leukocyte responses to infection or injury
(leukocytoses relating to these)

Back 44

-bacterial infx: - increased granulocytes, most neutrophils (granulocytes = neutrophils,basophils,eosinophil)
-viral infxn: - lymphocytosis
-parasites & allergic rxns: -eosinophilia

Front 45

band neutrophil

Back 45

-least mature WBC, normally bound in peripheral blood (less than 5% of WBC count)
-has banana shaped nucleus
-left shift- clinically referred to as released of immature cells
-don't usually appear in blood unless leukemia is present

Front 46

infectious mononucleosis

Back 46

-caused by Epstein-Barr virus
-infects B lymphocytes, typically causes fever, sore throat, enlarged jaw/neck lymph nodes, & incr lymphocytes in peripheral blood
(many are large 'atypical' lymphocytes)
-blood of pts with mono will have HETEROPHIL antibodies
(coagulate red cells from other species)

Front 47

lymphadenitis

Back 47

-infection of lymph node, usually result of spread of organisms into nodes draining and infected site.
-if only reacting to infx; called reactive lymphadenitis/hyperplasia
-ACUTE: enlarged tender nodes neck/throat-->dental infxn, sore throat
-chronic: specific (to TB) & nonspecific (no etiology known)

Front 48

catscratch disease

Back 48

acute lymphadenitis caused by a rickettsia-like micororganism Bartonella henselae
-acute syndrome of axillary & neck lymphadenitis in children & teens -->2 weeks p catscratch

Front 49

what are the kinds of lymphoid neoplasms?

Back 49

lymphocytic leukemia,
lymphoma
plasma cell proliferations

Front 50

Lymphocytic Leukemia:
Acute LL

Back 50

-uncommon, malignant proliferation of immature lymphocytes, usually B-cells (children/teens)
-abrupt onset
-accompanied by widespread malignant cell infiltration of bones, lymph nodes, liver, spleen.
-causes bone pain, lymphadenopathy, hepatosplenomegaly
-infiltration of meninges (causes HA)
-chemo induces remission- 50% ultimately cured

Front 51

Lymphocytic Leukemia:
Chronic LL

Back 51

-malignant proliferation of B-cells that accounts for about 1/3 of all leukemias
-indistinguishable from SMALL CELL LL.
--except: CLL has few malignant cells in peripheral blood
-gene defect that stops lymphocyte apoptosis
-as malignant B-cells proliferate, normal B cells vanish & pts prone to infxns.
-sluggish of all leukemias, occurs in adults
-wt loss, fatigue, poor appetite
-Tx: chemo, avg survival 10 years or longer

Front 52

Lymphocytic Leukemia:
Small Cell LL

Back 52

-few malignant cells in peripheral blood
-gene defect that stops lymphocyte apoptosis
-as malignant B-cells proliferate, normal B cells vanish & pts prone to infxns.
-wt loss, fatigue, poor appetite
-Tx: chemo, avg survival 10 years or longer

Front 53

what are plasma cells?

Back 53

B-lymphocytes that are actively making antibodies (immunoglobulins)

Front 54

plasma cell dyscrasia

Back 54

-when a clone of a plasma cell begins to proliferate abnormally
-most plasma cell dyscrasias are malignant, but some benign
-malignant cell makes too much of its antibody--> result large amount of homogenous immune protein in blood circ.
-protein appears as dense band in gamma globulin region in electrophoresis (called MONOCLONAL SPIKE)

Front 55

Bence-Jones Protein

Back 55

-when plasma cell proliferation makes heavy or light chains
-light chains are liberated by breakdown of M-proteins, and are small enough to pass through glomerulus into urine... BJ proteins
(can be nephrotoxic)

Front 56

Multiple Myeloma

Back 56

malignant proliferation of plasma cells
-do not circulate in blood, appear as nodular masses in bone marrow
-they destroy bone, produce 'punched out' bone defects (especially in spine and skull)
-decline in production of normal immunoglobulin/antibodies & suspect. to infxns
-occurs in elderly --bone pain, hypercalcemia, and anemia common complaints
dx: x-ray
prognosis: poor, chemo is usually not effective. 3 year survival

Front 57

Waldenstrom macroglobulinemia

Back 57

-a cross between multiple myeloma and small cell LL
-malignant cells look like lymphocytes
-affects >60y/o, symptoms: anemia, wt loss, fatigue, weakness, lymphadenopathy, splenomegaly
-IgM is thick and syrupy causes sluggish blod flow --> causes dizziness, confusion, stroke, visual symptoms
-survival few years, similar to multiple myeloma

Front 58

Lymphoma
basics, 2 types

Back 58

-malignant neoplasms of LYMPHOCYTES or
-->lymphoblasts that grow as nodular masses (usually in lymph nodes)
2 broad types:
Hodgkin's
and
all the rest: Non-hodgkin's

Front 59

HODGKIN Lymphoma

Back 59

-malignant cell = lymphoid cell (arises in lymph node) known as Reed-Sternberg cell,
-theory-it becomes malignant from infxn of EBV
-most common malignant neoplasm of Americans b/w 10-30 y/o
-M>F (twice as frequently in W as in AA's)
-immunocompromised pts have higher tendancy to develop
-pts with HL tend to have poor T-cell immunity (develop infxns)
--HL first manifestation: painless nontender enlargement of lymph nodes, often in neck.
-wt loss, fatigue, fever, night sweats, fatigue
-in 10% alcohol causes pain
--Radiation tx & chemo tx --> permanent remission, 5 yr survival

Front 60

Hodgkin Lymphoma differs from NHL in what 3 ways?

Back 60

-HL arises in a single LYmph node or chain of nodes & spreads in an orderly, preditcable manner to adjacent nodes (rather than spreading widely like NHL does)
-HL rarely involves structures other than lymph nodes
-all types of HL are associated with defective cell-mediated (T-cell) immunity (manifested by infxns)

Front 61

nodular Sclerosis Hodgkin Lymphoma

Back 61

-accounts for 70% of cases
-differs from HL by:
--it is is only variety of HL that is more common in women than men
--has conspicuous tendancy to involve neck, upper chest, mediastinal lymph nodes
--least aggressive

Front 62

NonHodgkin Lymphoma

Back 62

-most are malignant tumors of B-lymphocytes
- more aggressive, and in more advanced clinical stage at time of dx, microscopic behavior vary greatly from one type to the next
-1/3 arise from organs like brain, bone, bowel. spread widely.

Front 63

Pathological classification of NHL

Back 63

-very complex classificaion by WHO
-simpler method::
->2 main groups
--follicular lymphoma
-->diffuse lymphoma

Front 64

more on Follicular lymphomas

Back 64

-follicular lymphomas are less aggressive and have a better prognosis than diffuse lymphomas
--arise as painless enlarged lymph nodes
-median survival 10 years
-do not respond well to chemotx

Front 65

more on diffuse lymphomas

Back 65

half of all NHL are diffuse
-in pts >60y/o: 2 exceptions:
-childhood & AIDS
-appear quickly, grow rapdily, lethal unless treated.
-s/p chemo: 30% pts permanent remission
-most temporary complete remission

Front 66

Small cell lymphocytic Lymphoma

Back 66

-lo grade diffuse lymphoma (in connection to chronic lymphocytic leukemia)
-essentially same disease: except::
--> in scLL the peripheral blood lymphocyte count is low.
(the opposite is true in CLL)

Front 67

Clinical features of non-Hodgkin Lymphoma

Back 67

-enlarged non-tender lymph nodes
-incr metabolic rate responsible for fever, wt loss, malaise, sweating
-autoimmune phenomena or immunodeficiency problems such as infection

Front 68

acute myelocytic leukemia

Back 68

--malignant proliferation of immature granulocyte precursor cells, do not mature enough to develop neutrophilic, basophilic or eosinophilic granules
-all have gene mutations that prevent cells from maturing --> immature cells overrun blood/marrow
-disease of middle-aged/older adults,
-onset sudden, symptoms of marrow failure (because malignant cells crowd out normal marrow) and red cell & granulocyte counts fall -->anemia, hemorrhage, infxn
symptoms: bone pain, anemia, lymphadenopathy, liver/spleen enlargement
-chemo tx remission in 2/3 younger pts. older 10% 5 yr survival

Front 69

chronic myeloproliferative disorders

Back 69

-related neoplastic diseases, all of which arise from myeloid stem cells: all have tendency toward Acute myelocytic leukemia
4 disorders (org. by way stem cells differentiate)
--polycythemia vera (malignant red cells dominate)
--chronic myelogenous leukemia (malignant granulocytes dominat)
--malignant thrombocythemia (megakaryocytes predomnte)
--myeloid metaplasia w myelofibrosis (cells differentiate toward fibrous tissue)
2 FEATURES COMMON TO ALL:
-->myelofibrosis & extramedullary hematopoiesis

Front 70

Myelofibrosis

Back 70

-replacement of normal bone marrow by fibrous tissue that grows as a result of fibrogenic factors released by nepolastic megakaryocytes
-appears as final, fatal phase in many chronic myeloproliferative syndromes
-severe anemia, thrombocytopenia & leukopenia result in hypoxia, bleeding, infection

Front 71

Extramedullary hematopoiesis

Back 71

production of blood cells in organs other than the bone marrow
-most in liver/spleen
-red cells tend to be deformed, released before losing nucleus
-hepatosplenomegaly

Front 72

chronic myelocytic leukemia

Back 72

affects middle aged adults, 15% of adult leukemias,
slow onset, worses progressively
-fever, malaise, wt loss, weakness, anorexia
-splee is huge
-(in contrast to acute ML) most of the malignant cells are mature neutrophils, but some eosinophils & basophils are present
-WBC counts very high
chemotx: 90% survive 3 years, half can be consrd cured

Front 73

polycythemia vera

Back 73

chronic myeloproliferative : red cell precursors predominates
-usually accompanied by limited overgrowth of granulocytes & megakaryocytes
-red cell elements predominate & absolute incr of total red cell mass, red cell counts, & elevated H/H
-appears slowly in middle-age adults as vague constitutional symptoms: intestinal bleeding, gout, HTN, pruritus, flushed complexion.
-some pts tend toward DVTs, long evolution of disease: decade to burned out state (same features as myelofibrosis w. myeloid metaplasia)
conclusive dx: requires total red cell mass

Front 74

malignant thrombcythemia

Back 74

aka - essential thrombocythemia
rare, chronic myeloproliferative,
predominant cell is megakaryocyte
-platelet counts very high
-dx is one of exclusion (since all myeloproliferative syndromes have high platelets)
-circulating giant platelets common
-myelofibrosis absent. thrombosis & hemorrhage most common clinical problems. sluggish disorder w/ periods of quiet. survival 10-15 yrs

Front 75

myeloid metaplasia with myelofibrosis

Back 75

myeloproliferative in which marrow fibrosis predominates.
-caused by release of fibrogenic factors from neoplastic megakaryocytes
-occurs in older adults, most w/ large spleens.
-red cells made outside marrow tend to be deformed & retain nuclei.
-giant platelets, incr basophil count, incr uric acid.
pts suffer hemorrhagic thromotic problems. final phase is "blast crisis". evolves rapidly into acute myeloid leukemia. few year survival.

Front 76

myelodysplasia

Back 76

group of bone marrow stem cell proliferations characterized by **ineffective RBC production**
cases occur spontaneously in older adults/result of chemotx/radtx
-->also referred to as "preleukemia" and "smoldering leukemia"
-marrow is hypercellular & contains many dysplastic red & white cells
-red cell esp is impaired, gives rise to refractory anemia
survival = a few years

Front 77

describe the normal functions of endothelial cells

Back 77

they control diffusion of a substances across the vascular wall into adjacent tissues
-maintain blood in a smooth clot-free state

Front 78

classify plasma lipids:

Back 78

classified:
-chemically
-density
-->chemically plasma lipids are either cholesterol or triglyceride and circulate to an attached protein. (the apoprotein) to form a lipoprotein
--classified by density into high-density Lipoproteins, low density lipoproteins, and very-low density lipoproteins.
-each type contains varying amounts of cholesterol and triglyceride

Front 79

explain why 'normal' is not a useful concept in study of plasma lipid levels

Back 79

the concept of "normal" is misleading because it relies on the average cholesterol of presumably healthy people, and the average cholesterol in the US is unhealthily high
"desirable" is a better descriptor for healthy levels of plasma lipids

Front 80

explain the difference between atherosclerosis and arteriosclerosis

Back 80

atherosclerosis is a lifestyle disease of large & medium sized vessels characterized by fatty deposits in vascular walls
Arteriosclerosis is a disease of small blood vessels mainly seen in DM and HTN (no fatty deposits are involved)

Front 81

name the pathologic process important to the formation of an atheroma

Back 81

the important processes are:
-endothelial damage
-lipid accumulation
-inflammation
-smooth muscle cell migration
-fibrosis

Front 82

list the factors that predispose to atherosclerosis & name some indicators of risk

Back 82

smoking, obesity, lack of exercise, and high-salt, high-fat diets

Front 83

name the most important clinical complications of atherosclerosis

Back 83

myocardial infarct, stroke, aneurysm, and peripheral vascular disease

Front 84

discuss the pathologic differences between young & old atheromas

Back 84

young atheromas are dangerous because they tend to be fatty, soft, and unstable-- they are prone to ulceration, hemorrhage, and thrombosis.
OLD atheromas are fibrotic, hard, & sometimes calcified. they are less dangerous & are stable & may cause downstream ischemia, but they are not prone to thrombosis and sudden occlusion

Front 85

name the 2 main components that determine blood pressure

Back 85

peripheral resistance and cardiac output

Front 86

name & define the 2 main major types of hypertension

Back 86

Essential (Primary) is NOT associated with any identifiable underlying causative condition.
Secondary HTN is HTN that is related to a specific underlying condition

Front 87

name the characteristic kidney findings in HTN

Back 87

benign nephrosclerosis with hyaline arteriosclerosis

Front 88

give a clinical definition of HTN

Back 88

sustained diastolic blood pressure of 90 mmHg or greater or sustained systolic pressure of 140 mmHg or greater

Front 89

name the cause of most aneurysms

Back 89

atherosclerosis, which weakens the vascular wall and allows the affected vessel to dilate

Front 90

name the most common basic mechanism of vasculitis

Back 90

autoimmunity

Front 91

briefly explain Raynaud phenomenon

Back 91

it is an exaggeration of normal vasoconstriction and vasodilation reaction to cold or stress manifested by blanching and later cyanosis.
it usually appears in the fingers

Front 92

explain the clinical importance of thrombophelbitis

Back 92

-thrombophlebitis is a combination of venous thrombosis and vein inflammation.
-it is a common condition that usually occurs in deep leg veins.
-thrombi of any size can embolize.
-most travel to the lungs, where they lodge and obstruct pulmonary artery blood flow & can cause lung infarction.
-a large embolic thrombus can completely occlude the pulmonary artery & cause sudden death

Front 93

hypersplenism

Back 93

overactivity of splenic function
-most common viral infection, chronic autoimmune disease, malaria, lymphoma, leukemia, chronic passive congestion owing to right heart failure & portal HTN (assoc w/ cirrhosis)
-enlarged spleen maybe overactive & remove more cells from blood than it normally should

Front 94

myasthenia gravis

Back 94

rare, acquired autoimmune diease
-->antibodies block transmission of nerve signals across the neuromusclar synapse
-half of cases have thymic hyperplasia or thymoma
(a tumor of thymic epithelial cells)

Front 95

excessive bleeding is caused by what 3 factors? (can be one of them)

Back 95

1-fragile small blood vessels
2- decreased platelet count or ineffective platelet function
3-decreased coagulation factor activity

Front 96

thrombocytopenia

Back 96

low platelet count
-characterized by tiny hemorrhages in skin or mucosae
-may occur when platelet production is low because of primary bone marrow disorder, toxic effects of drugs or chemicals (thiazide diuretics)
or ineffective platelet production (like in B12 def)

Front 97

immune thrombocytopenic purpura

Back 97

-more common cause of low platelet counts
-body destroys its own platelets
-occurs as isolated disease
-or complication of pediatric disease
-presents as sunungal or conjunctival petichiae
-splenectomy curative in most cases

Front 98

von Willebrand disease

Back 98

stems from deficiency of von Willebrand Factor (vWF) (made in endothelial cells)
-most common inhertied coagulation disorder, characterized by sponatenous bleeding from nose, mouth and other mucous membranes.
-bleeding time prolonged despite normal platelet count because of vWF

Front 99

Christmas disease

Back 99

hemophilia B, factor IX deficiency, clinically similar to classic hemophilia, much less common
-->
-caused by X-linked recessive gene defect (like classic hemophilia)
-may or may not be associated with bleeding problems

Front 100

DIC
disseminated intravascular coagulation

Back 100

-where all the clotting factors get used up. a 'consumptive coagulopathy'. usually characterized by hemolytic anemia. thromboses & hemorrhage. initiated by variety of factors:
-obstetrical
-infections
-neoplasms
-massive tissue trauma
-others: snake bite, heat stroke, acute hemolysis, vasculitis

Front 101

Lupus anticoagulant

Back 101

AKA - antiphospholipid antibody
-an autoantibody that occurs in about 10% of pts with systemic lupus erythematosus. are at increased risk for recurrent venous thrombosis. recurrent spontaneous abortions. most pts with lupus do NOT have SLE.

Front 102

Factor V Leiden

Back 102

abnormal form of coagulation factor V: produced by defective gene.
-promotes generalized tendancy to form venous thrombi.
-autosomal recessive defect.
- lab tests needed to confirm dx.

Front 103

Desirable Lipid values

Back 103

Total cholesterol <200 mg/dL
HDL cholesterol >60
LDL cholesterol <100
Triglyceride <150

Front 104

Lower total plasma cholesterol by 40 mg/dL...

Back 104

reduces cardiovascular risk by HALF, and each additional 40 mg/dL decrease cuts the risk in half again

Front 105

2 varieties of arteriosclerosis

Back 105

1-hyaline arteriosclerosis
2- hyperplastic ateriosclerosis

Front 106

hyaline arteriosclerosis

Back 106

a homogeneous thickening of arteriolar walls, is an inevitable part of the ageing process;
-->is accentuated by HTN and DM
most easily detected in afferent arterioles of renal glomeruli

Front 107

hyperplastic arteriosclerosis

Back 107

is onionskin hyperplasia of cells in arteriolar walls, mainly seen in the kidneys in VERY SEVERE (malignant) HTN

Front 108

what are the basic steps in pathogenesis of atherosclerosis?

Back 108

1-endothelial injury
2-lipid accumulation
3-influx of smooth muscle cells & macrophages
4-young atheroma
5 -old atheroma

Front 109

endothelial injury can result from:

Back 109

-hyperlipidemia
-HTN
-smoking
-Homocysteine
-viruses & other factors
-immune reactions

Front 110

factors in Endothelial cell dysfunction

Back 110

-increased permeability
-monocyte & platelet adhesion
-monocyte emigration

Front 111

how are arterial smooth muscle cells important in the development of atherosclerosis?

Back 111

-they react to the presence of lipids and inflammation & migrate into the developing atheroma where they change into fibrocytes that produce scar tissue, and into macrophage-like cells that engulf and store cholesterol

Front 112

dissecting hematoma

Back 112

-longitudinal tear due to defect in endothelial lining
(ulceration & atheroma)
-blood progresses along tissue planes
-reenters or ruptures

Front 113

2 most common causes of aneurysm ?

Back 113

-atherosclerosis
cystic medial degeneration (a degenerative condition of the vascular wall)
--> the abdominal aorta is the most common site of an atherosclerotic aneurysm

Front 114

things that can cause secondary HTN, elaborated

Back 114

-pheochromocytoma (tumor of the adrenal medulla that increases peripheral resistance by secreting vascoconstrictive horomones such as epinephrine
--tumor/hyperplasia of renal cortex: may produce excess steroid hormones (cortisol/aldosterone) which incr blood volume.
--renal disease; HTN may result from any kidney disease, impairs renal blood flow, lesions can be corrected surgically

Front 115

polyarteritis nodosa
pam is a small lady

Back 115

general, systemic AI disorder of small/medium sized arterioles leading to downstream ischemia.
-->kidneys are severely affected
-autoimmune disease of middle aged (women more than men)
-->think of Pam

Front 116

Takayasu arteries
fat japanese lady

Back 116

*larger* arteries (granulomatous inflammation of aorta)
-autoimmune disease of females less than 40
-present with poor perfusion of upper extremities

Front 117

temporal arteritis
old woman chewing

Back 117

(most common vasculitis)
-a LOCAL vasculitis
-chronic inflammation of temporal/cranial arteries
-->carotids, ophthalmic arteries
-70 years onward, older females
-headache, scalp tenderness, stroke, blindness
(associated with PMR 25%)
curable with steroids

Front 118

thromboangitis obliterans
(Buerger disease)

Back 118

-small vessels in hands/feet (extremities)
-cigarette smokers
-->leads to ischemia, ulcers, gangrene (think: smokers have yellow fingertips)

Front 119

what is vasculitis?

Back 119

general term that applies to group of uncommon diseases that feature inflammation of blood vessels, especially arteries
ex: polyarteritis nodosa, Wegner granulomatosis, necrotizing vasculitis.

Front 120

varicosity

Back 120

abnormal dilation of vein
--superficial leg veins
-->50 obese, women, multiparous, standing
-cosmetic: until dilation makes valves incompetent (lower extremity edema, stagnation of blood, ischemia, skin atrophy, & inflammation
-(stasis dermatitis)

Front 121

hemorrhoids

Back 121

varicose veins of anus,
they drain into portal system & may be seen in conjuction with cirrhosis of liver & portal venous HTN

Front 122

esophogeal varices

Back 122

varicose veins of esophagus mucosa
also occur with cirrhosis for same reason

Front 123

kaposi sarcoma

Back 123

malignant vascular tumor caused by uncommon type of herpes virus infexn in pts who are immunodeficient
-or are being treated with immunosuprressive drugs

Front 124

thrombophlebitis

Back 124

formation of venous thrombi, may be accompanied by inflammation of the vein
-deep veins of legs account for 90% of thrombophlebitis
-any condition that causes incr venous pressure can cause thrombi: pregnancy, heart failure, obesity, prolonged bed rest, burns, broken bones, other illness

Front 125

Discuss why cardiac arrhythmias decrease cardiac output

Back 125

arrhythmias are mechanically inefficient because chambers contract (beat) before they are optimally filled with blood

Front 126

define heart failure

Back 126

heart failure is mechanical failure of the heart to eject the volume of blood delivered to it

Front 127

explain the Frank-Starling curve and its importance

Back 127

-the Frank Starling curve is a graphical depiction of the relationship between cardiac muscle fiber length and strength of cardiac muscle contraction.
>up to a point as cardiac muscle fibers are stretched, they contract with MORE force; beyond that point the contractions weaken.
>in the failing heart, muscle fibers stretch & contract more forecefully as the heart fills with extra blood.
>this is a compensatory mechanism that helps the failing heart maintain competence

Front 128

explain the difference between forward and backward heart failure

Back 128

>the heart fails when it cannot eject blood delivered to it.
>a failing LEFT ventricle causes low cardiac output, commonly known as FORWARD failure.
>Left ventricular output lags & unejected blood dams up, congesting the lungs.
>this in turn makes it difficult for the R ventricle to eject its incoming load of blood.
>as a result, the R ventricle may fail.
>R ventricular failure is commonly called BACKWARD failure, which produces generalized venous congestion & edema.

Front 129

explain how & why renin is involved in heart failure

Back 129

>L heart failure results in LOW cardiac output, which causes LOW blood pressure & blood flow to the kidneys.
>the kidney responds by secreting additional RENIN, which stimulates the adrenal cortex to secrete aldosterone.
>Aldosterone in turn acts on the kidney, causing it to retain sodium & H20, thus explanding vascular volume.
>the expanded vascular volume increases cardiac work & makes cardiac failure worse.
>lowering cardiac output and causing even more renin secretion in a vicious circle.

Front 130

contrast the clinical findings & symptoms of Right HF and Left HF.

Back 130

LEFT HF: pulmonary congestion & edema. SOB, fatigue, tachycardia, & ENlarged heart, congested edematous lungs.
pure RIGHT HF: symptoms above are absent, (but most common cause of R HF is left HF so both are often present together). sx=systemic congestion, dependent edema in the feet, legs, genitals, hepatosplenomegaly, ascites, & pleural effusion. additional complications: deep venous thrombi, pulmonary thromboemboli.

Front 131

name the syndromes of ischemic heart disease

Back 131

-angina pectoris
-myocardial infarction
-sudden cardiac death
-chronic ischemic heart disease (ischemic cardiomyopathy)

Front 132

explain why YOUNG atheromas are more dangerous than older ones are

Back 132

>young atheromas are soft & prone to fissure, rupture, or hemorrhage.
>each may precipitate thrombosis, & coronary occlusion.
>Older sclerotic (sometimes calcified) plaques, are likely to produce ischemia/angina are not prone to a sudden occlusion & infarction & are easier to identify by diagnostic imaging.

Front 133

explain why prompt intervention may limit the size of an infarct

Back 133

>infarcts do not leap into being instantly. they evolve from smaller to larger.
>the first muscle to die is at the end of the coronary vascular supply. (subendothelial muscle)
>infarct gradually enlarges for several hours until it is complete
>prompt therapeutic intervention to reestablish coronary flow may stop necrosis while the infarct is small

Front 134

list some complications of myocardial infarct

Back 134

>sudden death
>CHF
>cardiac rupture
>mitral regurgitation
>arrhythmia
>mural thrombus
>thromboembolism
>cardiogenic shock

Front 135

contrast the symptoms of myocardial infarct & angina

Back 135

>both angina & myocardial infarct have pain with similar distribution
(substernal with radiation to left arm or jaw/other sites)
ANGINA: may be relieved by rest or medication.
MI: pain is unremitting. also pts may sweat profusely, have nausea, vomit & have dyspnea.

Front 136

explain the usefulness of cardiac creatine kinase (CK-MB) & cardiac troponin assays in the assessment of chest pain.

Back 136

>there are distinctive molecular elements of cardiac muscle that are washed into the bloodstream in a MI & can be detected by lab tests
>NO cardiac damage occurs with angina.

Front 137

discuss effects on heart of chronic hypertension:

Back 137

>the strain imposed by pumping against high pressure causes LEfT ventricular hypertrophy
>hypertrophic myocardium is stiff and has higher-than-normal metabolic requirements, which makes the muscle more susceptible to infarction at any given amount of coronary obstruction.
>stiffness reduces ventricular movement (compliance) & stroke volume & increases the distance over which oxygen & nutrients must diffuse through the ventricular wall.
>also: chronic HTN predisposes to coronary atherosclerosis.
>end result is often CHF, MI & cardiac arrhythmia.

Front 138

explain the difference between valvular stenosis & valvular insufficiency.

Back 138

>a STENOTIC valve is one which fails to open FULLY, obstructing easy passage of blood.
>an INSUFFICiENT valve is one in which the valve leaflets have lost part of their one-way gate function -either: they don't close completely or have defects that allow backflow.
>BOTH stenosis & insufficiency are mechanically inefficient.

Front 139

Briefly explain the pathogenesis of Acute Rheumatic Fever
&
Rheumatic Heart disease

Back 139

>acute rheumatic fever: an autoimmune disease that occurs in some cases of group A streptococcal pharyngitis.
> where anitibodies against strep antigens the similar self antigens that are found in heart & joints
>the immune attacks may be chronic & subclinical (silent) and cause chronic rheumatic valvulitis

Front 140

explain the difference between infective endocarditis & nonbacterial endocarditis
& know the hazards associated with each:

Back 140

>INFECTIVE endocarditis: is infection, usu. bacterial, of heart valves. oft. assoc w/ IV drug abuse, chronic rheumatic valvulitis or prosthetic valves. EroSion of valve produces valvular regurgitation (insufficiency) which can occur ACUTELY and CATASTROPHICALLY. bacterial emboli may cause distant abscesses; ex: in the brain.
>NONBACTERIAL thrombotic endocarditis: condition where fibrin & platelets accumulate on valve leaflets as small vegetations. seen in: cachexia, internal malignancy, DVT, & others. risk of these is: become infected or embolize to cause infarction, esp; brain infarcts

Front 141

Define:
Primary Cardiomyopathy & offer several examples:

Back 141

Primarly cardiomyopathy is INTRINSIC disease of the cardiac muscle
>caused by inflammation,
metabolic disorder,
autoimmune disease,
or muscular dystrophy/other genetic conditions.
-some are unknown causes

Front 142

Explain why congential cardiac malformations with L to R shunts can cause pulmonary HTN & late cyanosis

Back 142

Pulmonary HTN arises when incr. volume of blood under high pressure is shunted thru the pulmonary artery & lungs from the LEFT side of the heart.
>if pulmonary pressure rises markedly, RIGHT side pressure may exceed LEFT side pressure & causes reversal of blood flow (and late cyanosis) thru the defect.

Front 143

Major Determinants of Heart Disease

Back 143

Most heart disease is the result of atherosclerotic obstruction of the coronary arteries.
•! Congestive heart failure is mechanical failure of the heart to eject blood delivered to it.
•! Metabolic or autoimmune disease may cause heart muscle or valve damage.
•! High blood pressure accelerates atherosclerosis and most other cardiac disease.

Front 144

Major Determinants of Heart Disease
Continued

Back 144

-Cardiac valves are one-way gates for blood flow and are susceptible to obstruction and regurgitation (incompetence).
•! Cardiac valves are susceptible to infection. •! Abnormal embryonic development of the heart produces
significant cardiac anatomic malformations.
•! Abnormal heartbeat patterns (arrhythmias) can cause cardiac dysfunction or death and can complicate any heart condition.

Front 145

Characteristics of normal form and function

Back 145

-! Beats paced according to demand
–! Normal beats are electrically separate
–! Signals begin in SA node and follow a certain path
–! Atria and ventricles electrically disconnected except for bundle of His
–! Every part of conduction system capable of self- stimulation
–! Cardiac muscle cells allow passage of signal cell to cell –! Cardiac fibers stay contracted for an instant before
relaxation and repolarization

Front 146

Arrhythmias: Electrical Mechanisms

Back 146

Reentry: signal loops back before new SA signal arrives
•! Faulty automaticity: abnormal focus of initial discharge
•! Electrically unstable cell membrane: electrolyte disorders, cardiac ischemia

Front 147

Sinus rate disorders

Back 147

bradycardia,
tachycardia,
arrhythmia,
sinus arrest

Front 148

Ectopic Impulse Origination (not in SA node)

Back 148

Escape Rhythms: slow, inefficient –! Premature atrial beats
–! Atrial flutter, atrial fibrillation

Front 149

Arrhythmias:
Junctional dysrhythmias ...
•! Ventricular dysrhythmias

Back 149

Premature ventricular beats –! Ventricular tachycardia –! Ventricular fibrillation

Front 150

Atrioventricular block:

Back 150

1st degree: slow
–! 2nd degree: some signals do not get through
–! 3rd degree: no signals get through

Front 151

Accessory pathways:

Back 151

AV node bypassed (Wolff- Parkinson-White)

Front 152

epicardium

Back 152

the transparent membrane on the heart surfaca

Front 153

endocardium

Back 153

-all chambers in the heart lined with it
-thin cellular membrane that is a continuation of the vascular endothelium which also lines blood vessels

Front 154

how are arrhythmias caused?

Back 154

-caused by myocardial ischemia or myocardial infarct,
-electrolyte imbalance (esp K+)
-stress
-caffeine
-drugs (esp stimulants)
-congenital defects in myocardial electrial network

Front 155

atrial flutter

Back 155

rapid organized REGULAR atrial rhythm near 300/min
& regular ventricular rate of about 150-200 /min

Front 156

atrial fibrillation

Back 156

disorganized irregular atrial rhythm that causes an irregular rapid ventricular rate near 200/min
>>leads to drop in CO, pts c/o dizziness & fatigue
>long term risk of atrial thrombi that can embolize & go for the brain

Front 157

risks of heart disease & stroke

Back 157

>1/3 deaths in US from coronary artery atherosclerosis

(if including CVA and DM complications & others gets up to >40%)
>lifetime risk for CAD:
men = 50% women = 40%

Front 158

uncompensated HF

Back 158

-when heart fibers stretched too far, force of contractions weaken, and cardiac output falls
(blood backs up like water behind a dam) >> heart goes into UHF

Front 159

2 components of Uncompensated Failure:

Back 159

Forward Failure: low ventricular output
Backward Failure:venous congestion

Front 160

cor pulmonale

Back 160

>pure right heart failure, is uncommon
associated with pulmonary HTN (resulting from vascular diseases)
>most common cause is left heart failure

Front 161

what is the most common cause of Left Heart Failure?

Back 161

-damaged cardiac muscle, usually associated with coronary atherosclerosis, with ischemia or infarction
>can also be caused by excess strain of high blood pressure (HTN) or aortic/mitral valve disease

Front 162

Features of CHF
(left HF)

Back 162

-most prominent: breathlessness (dyspnea) esp during activity
-prominent pulmonary veins
-enlarged cardiac silhouette
-rapid heart rate
-pulmonary edema (heard by rales in lung bases)
-mitral regurgitation
-atrial fibrillation

Front 163

Features of CHF:
(right HF)

Back 163

-incr venous pressure/engorgement of with blood
-distended neck veins
-edema in feet/genitals
-congestive liver/spleen enlargement
-accumulations of fluid in peritonium & pleura
-FataL: due to hypoxia, acidosis, cardiac arrhythmias

Front 164

how does ischemic heart disease arise?

Back 164

>atherosclerotic narrowing/complete occlusion of one or more coronary arteries

Front 165

clinical syndromes of ischemic heart disease

Back 165

-angina pectoris (chest pain)
-myocardial infarction
-sudden cardiac death
-chronic ischemic heart disease w/ CHF

Front 166

number 1 cause of death in US

Back 166

CORONARY ARTERY DISEASE

Front 167

stable angina

Back 167

rises & falls smoothly over a period of a few minutes and is relieved by rest or medication
>may be precipitated by exertion/emotion or by heavy meal or sudden exposure to cold
(rarely spontaneous)

Front 168

unstable angina

Back 168

>caused by aggregates of platelets accumulating on an atherosclerotic plaque
VERY serious condition may HERALD impending MI!!
>characterized by either:
1-intensification of existing angina
2-new onset of angina-at-rest
3-nocturnal angina
4-onset of prolonged angina

Front 169

Unremitting Angina

Back 169

angina that does not fluctuate & cannot be relieved by therapy
>caused by myocardial infarction
>accompanied by additional signs & symptoms

Front 170

what are most MI's initiated by?

Back 170

-plaque disruption (rupture, ulceration/ hemorrhage)
-accompanying THROMBOSIS
(coronary thrombosis) in severely atherosclerotic arteries

Front 171

infarction location, size & growth

Back 171

-the last muscle to be supplied is deepest in the wall
-the SUBENDOCARDIAL muscle is the first to die when infarct begins to develop
-begin as area of subendocardial infarction & continue to enlarge for 3 to 6 hours until it becomes full thickness (a transmural infarct)

Front 172

what is a mural thrombus?

Back 172

-a blob of:
>substances from dead/necrotic muscle ooze across endocardium which attracts PLATELETS, and WBC forming a mural thrombus
>>creates big risk for cerebral embolization & CVA

Front 173

cardiac tamponade

Back 173

- blood dissecting through soft, dead myocardium ruptures it
-creates acute hemopericardium with fatal cardiac smothering

Front 174

what is a much more specific marker than CK in identifying MI?

Back 174

Troponin: there are 2 types cardiac 1 and cardiac troponin T.
-neither is present in blood of healthy people.
-detection of small amounts is a sensitive AND specific indicator of MI

Front 175

most common cause of instantaneous death in the West?

Back 175

ischemic heart disease

Front 176

what are some causes of valvular insufficiency?

Back 176

-syphilitic aortitis
-myxomatous degeneration of aortic valve
-ruptured mitral valve chordae tendinae
-massive left ventricular dilation

Front 177

cardiomyopathies, more on kinds & basics

Back 177

>primary - intrinsic disease of cardiac muscle
>secondary - assoc with ischemic heart disease, infections, acquired metabolic disturbances/valvular disease, congenital or nutritional or immune system def.
>dilated/congestive- heart hypertrophy, dilation low EF, assc w/ alcohol & chemo
>hypertrophic - heart hypertrophy, gene defect/idiopath
systolic contractions are powerful
>restrictive-rarest, stiff noncompliant ventricle fills incompletely, systole is not forceful.

Front 178

congenital heart disease

Back 178

-cause is mostly unknown, environmental/genetic in 10% of cases
-defects develop in 1st 10 weeks
-3 types anatomically:
--malrotation, expansion, septal

Front 179

cardiac malformations & fetal circulation

Back 179

major difference between adult/fetal circulation:
-oxygntd blood flows in veins from placenta to heart
-oxy and deoxy blood is mixed in most of circulation
-little blood flows thru lungs, is shunted by passing from R atrium to L thru foramen ovale & from pulmonary artery to aorta thru ductus arteriosus

Front 180

left-to right- shunts

Back 180

most common type of congenital heart defect
>oxy blood from left side to right side. lead to pulmonary failure & r-side HF.
>3 main types: atrial septal defect, veintricular septal defect, patent ductus arteriosus.

Front 181

right-to-left shunts

Back 181

less common, there is malrotatiion of embryonic chambers.
>charactrzd by early cyanosis
>most common type:
Teratology of Fallot:
--ventricular septal defect
--small pulmonary artery or pulmonary valve stenosis
--misplaced aorta
--right ventricular hypertrophy

Front 182

transposition of great vessels

Back 182

second most common type of cyanotic heart disease
>aorta rises from right ventricle and pulmonary artery from the left, is incompatible with life.
>only that survive have some other defect that allows them to do so.

Front 183

coarctation of the aorta

Back 183

one of most common congenital diseases: has ring-like fibrous narrowing of the aorta, usually in aortic arch near ductus arteriosis.
>assoc with high BP in Uextremities
>low blood flow to kidneys, stimulates renin etc.
>pressure higher in pulmonary artery than in aorta, so deoxy blood flows into aorta below obstruction & produces cyansosis of lower body

Front 184

pericarditis

Back 184

most often caused by viral infection
>characterized by atypical chest pain and audible friction rub
>pericardial effusion may occur in non-inflammatory conditions
-Hemopericardium: undiluted blood in pericardial sac

Front 185

MCV (mean cell volume)

Back 185

average SIZE of a RBC

Front 186

MCH (mean cell hemoglobin)

Back 186

average AMOUNT of hemoglobin in the RBC

Front 187

MCHC (mean cell hemoglobin concentration)

Back 187

-average CONCENTRATION of hemoglobin per unit of volume in an average RBC

Front 188

anemia in a man or post-menopausal woman is considered...

Back 188

to be bleeding from a gastrointestinal cancer until proven otherwise

Front 189

Describe the pulmonary Interstitium

Back 189

-the pulmonary interstitium is the tissue lying between avleolar walls:
(that is, beneath the pneumocytes that line the alveoli)
--it consists of a thin network of pulmonary capillaries, basement membrane, fibrocytes, and smooth muscle cells, and collagen & elastin fibers

Front 190

Explain Spirometry, and name & explain the 2 spriometric measures critical to understanding lung disease

Back 190

Spriometry: measures the volume of air in the lungs, and airflow rates.
>>Forced vital capacity (FVC) is a volume measurement. --the volume of air expelled between a maximum inhalation and a maximum expiration.
--FEV (forced expiratory volume) is a RATE measurement. the volume of air flowing out of the lungs by forced expiration in the first second from a start at maximum inspriation

Front 191

name 2 risk factors for laryngeal carcinoma

Back 191

smoking
alcohol abuse

Front 192

name the types of atelectases

Back 192

-resorption
-compression
-contraction

Front 193

Define Asthma
briefly discuss underlying pathology

Back 193

-ashmat is a chronic inflammatory disease of small bronchi and bronchioles characterized by airflow obstruction resulting from bronchospasm. (which is a constriction of bronchioles b/c of smooth muscle contraction)
-the pathologic lesion in asthma is bronchial inflammation, sometimes associated with allergy, but caused in most cases by inhaled irritants (cigarette smoke/polluted air)
-regardless if it's allergic/environmental, with repeated exposure the reaction evolves into progressively severe chronic inflammation

Front 194

what are the 2 main categories of chronic obstructive pulmonary disease?

Back 194

chronic bronchitis
and
emphysema

Front 195

explain how chronic bronchitis and emphysema differ

Back 195

-both are obstructive airway diseases, smoking is usual cause of each.
>in "pure" emphysema the problem is coalescence of small alveoli into large airspaces, which decreases amount of alveolar membrane that can exchange gas.
>in "pure" chronic bronchitis, the pathologic lesion is bronchial inflammation and hypertrophy of mucous glands w/ exaggerated mucous secretion, which both combine to produce airway obstruction, the diffusion capacity of membrane is unaffected

Front 196

Define: Bronchiectasis

Back 196

-permanent dilation of distal bronchi and bronchioles caused by recurrent necrotizing bronchial infections that destroy supporting tissue of the airway, laving a dilated flaccid pus-filled tube

Front 197

define: restrictive lung disease,
explain pathogenesis

Back 197

RLD: limits both volume of lung expansion and contraction.

>restrictive lung diseases are chronic inflammatory conditions of pulmonary interstitial tissue that make the lung stiff/inelastic

Front 198

name 2 basic causes of pulmonary edema, give examples

Back 198

-Hemodynamic edema (in CHF)
-microvascular injury (as in inhalation of toxic fumes)

Front 199

what are the consequences of pulmonary thromboembolism?

Back 199

>repeated small pulmonary thromboemboli may occlude pulmonary arterioles to produce chronic pulmonary HTN
>larger emboli may produce lung infarcts
>very large emboli may occlude the pulmonary artery and cause instantaneous death

Front 200

name & discuss the 2 main anatomic varieties of pneumonia

Back 200

1Alveolar Pnuemonia: inflammation, usu. acute, severe enough to completely fill (solidify/consolidate) large numbers of alveoli w/ inflammatory exudate.
2>Interstitial Pneumonia: inflammation that is confined to the alveolar septa & does not fill the alveoli w/ inflammatory exudate. The inflammation is diffuse & bilateral, usually caused by viral infexn.

Front 201

Explain terms:
'community acquired pneumonia'
and
'nosocomial pneumonia'

Back 201

CAP: is acute pneumonia not acquired in some special circumstance, such as in a hospital/association with immune deficiency/aspiration of gastric contents
NP: pneumonia acquired in a hospital

Front 202

explain how lung abscesses differ bacteriologically from most other abscesses

Back 202

-they contain several types of bacteria, most contain anaerobic bacteria, and most contain bacteria normally found in the mouth

Front 203

what's the difference between infection with the tuberculosis bacillus and the disease TB?

Back 203

>infection only means that the lungs have been seeded by the tuberculosis bacillus & the immune system has contained the infection to a small focus in the lung/or lungs & nearby mediastinal (hilar) lymph nodes.
>Disease implies spread of infection beyond interstitial lung/lymph node lesions.

Front 204

why does 2ndary (reactivation) TB differ pathologically from primary progressive TB?

Back 204

2ndary (reactivation) occurs only in pts sensitized by earlier infection.
>as TB organisms spread the cellular (delayed, type 4) hypersensitivity reaction accounts for caseous necrosis, which occurs in 2ndary TB but not in primary progressive TB.

Front 205

classify malignant lung tumors by cell type

Back 205

2 main categories: small cell carcinoma, non-small cell carcinoma. (which consist of other types)
SCC: separated from other types b/c it is mUCH more aggressive than any other type.
NonSCC: cell types are: -squamous cell carcinoma, -adenocarcinoma,
-large cell carcinoma

Front 206

why is small cell carcinoma in a separate category from other lung malignancies?

Back 206

because SCC arises from neuroendocrine cells rather than bronchial epithelial cells
and
because it is uniformly lethal (even if discovered early)

Front 207

what 2 circulatory systems is the lung served by?

Back 207

-pulmonary
-bronchial
>pulmonary consists of pulm a. and veins & connecting capillaries in alveolar wall, provides nourishement to alveoli only.
>trachia & bronchi are nourished by bronchial arteries, which are branches of the thoracic aorta

Front 208

obstructive lung disease is characterized by:

Back 208

limitation of AIRFLOW
>the rate of air flowing out of the lungs is slowed, therefore the amount that can be expelled is low,
>lung volumes are usually normal (ratio of airflow to lung volume is low)

Front 209

restrictive lung disease is characterized by:

Back 209

-limitation of lung expansion
>the ratio of air flow to lung volume is usually near normal because restrictive disorders limit BOTH volume and flow rate proportionally
(the FEV/FVC ratio remains near normal range)

Front 210

atelectasis

Back 210

is lung collapse.
there are 3 types:
>resorption: when bronch obst. prevents air from reaching alveoli beyond obstruction. most common cause is a mucous plug formed during general anaesthesia
>compression: external pressure is exerted on lung from pleural blood, fluid, or air from upward abd. pressure on diaphragm
>contraction: when scars in lung/pleura constrict & collapse lung (irreversible, the first two are)

Front 211

right middle lobe syndrome

Back 211

-right middle lobe undergoes atelectasis b/c the bronchus is obstructed.
-r-lobe is served by an unusually long thin bronchus that is prone to obstruction from mucus/inflammatory debris.

Front 212

alpha-1-antitrypsin

Back 212

-a protein in the lung normally inhibited by proteins made in the liver that prevents digestive enzymes from dissolving tissue.
-smoking inhibits this enzyme thus leaving the lungs vulnerable to auto-digestion.

Front 213

bronchiectasis

Back 213

-marked, permanent dilation of small bronchi when there is destruction of smooth muscle & elastic supporting tissue of the airway
-leaves dilated, flaccid pus-filled tube.
-both obstruction & infection are required. is always a 2ndary condition to others like:
-immunodeficiency,
-chronic infections (TB)
-retained bronchial foreign body
-CF & other conditions

Front 214

idiopathic pulmonary fibrosis

Back 214

-mysterious disease, unknown etiology. most are middle aged adults. strong suspicion that immune rxns play role.
-some have collagen-vascular disease as underlying cause
-fibrosis begins insidiously, presents as SOB. cor pulmonale and hypoxia & cyanosis = advanced disease. some cases may regress but most have 5 year survival rate. Txp is only tx.

Front 215

Pneumoconiosis

Back 215

lung disease caused by inhaled dusts and fumes.
-coal dust causes black lung disease, rock or stone dust = silicosis

Front 216

asbestosis

Back 216

-lung disease cased by inhaled asbestos particles
-causes pulmonary fibrosis, pleural fibrosis, pleural effusion, or pleural mesothelioma.
>it does not cause lung CA per se but promotes development of CA in smokers becuase it traps those carcinogens in the lung.

Front 217

sarcoidosis

Back 217

-systemic granulomatous disease, unknown cause. affects many tissues/features granulatomous inflammation.
>can develop in any organ: mostly in lungs/mediastinal lymph nodes. occurs more in AA.
>some recover, most develop lung dysfunction/eye problems.
>dx: depends on biopsy.

Front 218

hypersensitivity pneumonitis

Back 218

-T-cell mediated delayed hypersensitivity rxn (AKA allergic alveolitis).
lung biopsy reveals wides spread granulomatous inflammation.
-acute may present like 'flu'. chronic exposure can cause intersitial fibrosis

Front 219

common causative factors of pulmonary edema?

Back 219

-microvascular injury
-by inhaled toxic fumes,
-hot gases,

-septicemia, IV drug abuse

Front 220

Pulmonary thromboembolism

Back 220

-embolization of a thrombus from origin (usually in deep vein of knee/upper leg/pelvis) to pulmonary arterial system
-very common, cause more deaths than traffic accidents
-conditions that promote: surgery, CHF, birth control pills, prolonged bed rest, metastatic CA. AlSO:
-inherited tendancy toward DVTs
caused by genetic defect of coagulation V (factor V leiden)
-lupus anticoagulant.
-recurrent subclinical thromboembolism is a cause of primary pulmonary HTN

Front 221

pulmonary hypertension

Back 221

-abnormally high blood pressure in pulmonary vascular tree
-most cases are 2ndary to:
-->COPD/interstitial lung disease
-->preexisting heart disease (shunts/mitral stenosis)
-->collagen vascular diseases
-->recurrent pulmonary thromboemboli

Front 222

Adult respiratory distress syndrome
(ARDS)

Back 222

-acute, bad disease
-something gets in lungs, neutrophils infiltrate, protein-rich exudate flows into alveolar space
-soB & rapid breathing dries the fluid into thick membrane that stiffens lung -->hypoxia
-causes: sepicemia, smoke, near drowning, oxygen toxicity, burns, heroin, DIC, pancreatitis, uremia, bone fractures of large bone.
-is fatal in 50% of cases. some who survive have permanent complications

Front 223

alveolar pneumonia

Back 223

-inflammation (usually acute) of alveoli, fills them with exudate.
-usually occurs w/ bacterial infxn
>-bronchopnuemonia: patchy non-contagious inflammation, involves alveoli of one lobe.
>-Lobar pneumonia: intense, consolidated acute inflammation of alveoli in entire lobe, more likely in pts with CHF, COPD, DM or alcoholism.
>Interstitial: confined to alveolar septa, diffuse, bilateral, caused by viral infexn.

Front 224

common organisms of community acquired pneumonia

Back 224

-Staph aureus
-H. influenzae
-Legionella pneumophila

Also: some by Mycoplasma pneumoniae, Mycoplasma rickettsia or virus.

Front 225

Ghon tubercle

Back 225

-initial lung lesion in primary TB.
-may be associated w/ similar lesions in infected mediastinal (hilar) lymph nodes
(known as Gohn complex)

Front 226

3 points about TB

Back 226

-many are infected, but few develop disease, about 95% of infxns are stopped by the lungs
-almost every clnical case of TB is 2ndary.
-when initially infected the immune system becomes sensitized and infection is halted.
later, infection may resurface with something that weakens immune system.

Front 227

epidemiology of TB

Back 227

-globally is second to AIDS in cause of infectious disease deaths
-Mantoux test (PPD test) skin test for prior infection.
-80% of population in some Asian/African nations have positive skin tests.

Front 228

primary progressive TB

Back 228

-5% of newly infected; infxn is not arrested goes on to widespread disease.
-sometimes associated with blood borne spread to other organs called 'miliary TB'.
-pts do not develop caseating granulomas b/c immune system has not be sensitized before.

Front 229

histoplasmosis

Back 229

-most common fungal infx in US.
-caused by H. capsulatum.
-endemic in Ohio river/central mississippi river (spread by inhaled dried bird droppings)
-Mantoux test is negative, helpful in differentiating TB from this.

Front 230

bronchiogenic carcinoma

Back 230

-most common of all human cancers
-#1 cause of cancer death for men/women.
-smoking cause.

Front 231

small cell carcinomas

Back 231

-20% of cases
-arise from neuroendocrine cells in bronchial epithelium
-smoking very closely tied
-agressively malignant, most pts have mets.grow fast, met early.
-are radiosensitive, are capable of secreting various hormones -->paraneoplastic syndrome

Front 232

Squamous cell carcinomas

Back 232

30% of cases
-malignant cells that differentiate toward type of flat cells that normally are found epithelium of skin, vagina and esophagus.
-most common in men, strong assoc with smoking.
-relatively slow growth arise centrally in main bronchi
-after becoming invasive have better prognosis

Front 233

Adenocarcinomas

Back 233

30% of cases
-most well differentiated lung CA
-have somewhat better prognosis than any of other types
-easier to remove surgically
-away from critical mediastinal structures
-arise in peripheral lung

Front 234

Large cell carcinomas

Back 234

15% of cases
-large fleshy round cells, lack differentiation.
-very poor prognosis, metastasize early.

Front 235

melena

Back 235

the passage of stool with high content of altered blood, which makes stool black

Front 236

hematochezia

Back 236

passage of overtly bloody stool

Front 237

hematemesis

Back 237

vomiting of blood

Front 238

rapid GI bleed

Back 238

-rapid GI bleeding is usually manifest by hematochezia or hematemesis or signs & symptoms of acute blood loss

Front 239

slow GI bleed

Back 239

-is often from an intestinal malignancy & tends to be clinically silent & without obvious evidence of blood in the stool. persistent slow GI bleeding is sometimes discovered b/c of the anemia it can produce

Front 240

what are stool occult blood tests good for?

Back 240

--> annual occult blood testing of stool detects many premalignant lesions of the colon before they become malignant
-->also detects many colon carinomas early enough for surgical care

Front 241

what is the difference between intestinal mechanical obstruction and ileus?

Back 241

intestinal mechanical obstruction: - normal intestinal function requires constant peristalsis: can be interrupted by mechanial obstruction or...

ileus: intestinal peristaltic paralysis

Front 242

what is the cause of the most tooth loss & explain its pathogeneis?

Back 242

-PERIDONTITIS causes the most tooth loss
-arises as a result of poor oral hygeine
-->which allows accumulation at the gum margin of a film of bacteria known as plaque
-->bacterial invasion downward into the soft tissues around the tooth root is the cause of peridontitis

Front 243

define: achalasia
what is it?

Back 243

--achalasia is a spastic condition of the lower esophogeal sphincter
--produces functional partial obstruction in the LE, causing dysphagia & esophogeal pain
--cause is unknown

Front 244

what is Barrett's esophagus, what is its pathogenesis? implications thereof?

Back 244

--Barret esophagus is a change (metaplasia) of the epithelium of the lowest part of the esophagus from NORmAL squamous epithelium to gastric glandular epithelium
-->Barret metaplasia is caused by: gastric acid refluxing upward from the stomach
-is painful, can cause bleeding & narrowing b/c of fibrous scar (stricture) -pts with BE have higher risk of esophageal adenocarcinoma

Front 245

what are some risk factors for esophageal carcinoma?

Back 245

smoking
alcohol abuse
Barrett metaplasia

Front 246

what are some conditions associated with H. pylori infection?

Back 246

-> chronic atrophic gastritis
->chronic peptic ulceration
->gastric carcinoma (usually in association w/ chronic atrophic gastritis)

Front 247

what is the pathogenesis of acute gastric erosions?

Back 247

-->acute gastric erosions are superficial ulcers of the gastric mucosa that are usually associated with severe trauma, sepsis, major surgical procedures, grave illnesses, alcohol abuse, extensive burns, CNS trauma/surgery & chronic exposure to NSAIDs & steroids.

Front 248

what is the pathogenesis of chronic peptic ulcerations?

Back 248

chronic peptic ulceration- is a much deeper ulceration of the stomach wall, may burrow into or through the muscular wall.
-peptic ulcers are assoc. with a combination of atrophic gastritis, exposure to gastric juices, and H. pylori infection

Front 249

what is the cause of Hirschsprung megacolon?

Back 249

-it results from a localized, genetic absence of the autonomic ganglionic neural plexus in the colon wall, which controls peristalsis.
-deprived of neural control, no peristalsis occurs in the affected segment, fecal movement is impaired, and the upstream colon distends with feces

Front 250

what is the most common cause worldwide of acute enterocolitis?

Back 250

Rotavirus

Front 251

what are some bacteria responsible for epidemic bacterial enterocolitis?

Back 251

-Salmonella sp. (causes salmonellosis)
-Shigella sp. (cause shigellosis)
-Vibrio cholerae (causes cholera)

Front 252

what is the pathogenesis of pseudomembranous colitis?

Back 252

-occurs with colonic overgrowth of C. difficile, which secretes an enterotoxin that causes necrosis of colonic mucosa.
-the most common cause is broad spectrum abx tx that kills normal colonic flora , allowing C. diff overgrowth

Front 253

malabsorption syndromes:
>luminal malabsorption

Back 253

intestinal malabsorption: consists of those cases in which a mucosal defect or disease is present that interferes with absorption, or in pts w/ shortened bowel

Front 254

malabsorption syndromes:
> intestinal malabsorption

Back 254

luminal malabsorption: caused by the absence of digestive enzymes or bile salts necessary for hydrolysis or emulsification of ingested foodstuffs (as in pts with pancreatic disease who do not have enough pancreatic enzymes for digestion)

Front 255

what are the differences between ulcerative colitis and Crohn's disease?

Back 255

1-type of inflammation: -granulomatous inflammation in Crohn's
-nongranulomatous in UC
2- depth of inflammation:
-deep transmural in Crohn disease
-superficial mucosal in UC
3-site of involvement:
-anywhere in the GI tract, but most often in the colon and terminal ileum in Crohn's,
4- continuity of inflammatory involvement:
-discontinuous (skips areas) in Crohn's,
-continuous in UC

Front 256

what are some extraintestinal manifestations of Crohn's and ulcerative colitis?

Back 256

-both may be assoc w/ uveitis
-joint disease
-skin disease
-inflammation of hepatic bile ducts (sclerosing cholangitis)

Front 257

what is the pathogenesis of colonic diverticulosis?

Back 257

-diverticular have a very thin wall composed of mucosa and submucosa only (no muscle)
-the mucosa & submucosa are extruded through the muscular wall at points where small arteries penetrate from the external surface
-colonic diverticulosis is uncommon outside of the West (hi fiber diets). from straining at stool causes incr. pressure in gut

Front 258

what is the importance of non-neoplastic polyps of the colon?

Back 258

-have no premalignant potential
-it is important to distinguish them from colonic adenomas, which are frequently polypoid & premalignant

Front 259

tubular adenoma

Back 259

- benign premalignant neoplasm
-has microscopic pattern of simple tubular glands & is commonly called adenomatous polyp

Front 260

villous adenomas

Back 260

-benign premalignant neoplasms
-less common
-broad-based, sessile polyp with a fern like microscopic pattern of epithelial growth that is called villous
-have much HIGHER malignant potential than tubular adenomas

Front 261

what is the relationship between colonic adenomas & colonic carcinoma?

Back 261

-almost w/out exception all carcinomas of the colon arise from preexisting benign colonic adenomas that gradually become dysplastic & then malignant over 10-15 years

Front 262

upper GI bleed

Back 262

-from esophagus, stomach or first few cm of duodenum where peptic ulcers usually appear
-may present as hematemesis, hematochezia, or melena
-most common causes: acute hemorrhage, gastritis, peptic ulcer of duodenum/stomach, esophogeal tears caused by vomiting, esophogeal varices, & vascular malformations

Front 263

lower GI bleed

Back 263

-originates anywhere in the bowel below the first few cm of the duodenum
-hematemesis is uncommon, blood usually appears rectally as hematochezia or melena
-in pts younger than 55 most common causes are:
-inflammatory bowel disease/colitis
-colonic diverticulosis
-neoplasms
-colonic angiodysplasia.
-in pts older than 55 the most common (excluding hemorrhoids) are:
-diverticulosis
-colonic angiodysplasia
-neoplasms
-inflammatory bowel disease or enterocolitis

Front 264

most common causes of ileus?

Back 264

-postop state after abd surgery
-appendicitis, gallbladder disease, peritonitis, other intra-abdominal diseases
-intestinal ischemia
-hypokalemia
-also assoc with pain, vomiting, lack of bowel movements (obstipation) & lack of bowel sounds

Front 265

most common causes of mechanical obstruction?

Back 265

-hernia (incarcerated hernia/strangulated hernia)
-adhesions
-intussusception (telescoping bowel)
-volvulus; a twisted segment of bowel on vascular stalk -->causes blood obstruction/ischemia/infarction
-also characterized by vomiting, abd. distention, lack of stools, hyperactive bowel sounds

Front 266

most important congential abnormality of oral cavity?

Back 266

cleft palate
/cleft lip
--malformations of embryological development

Front 267

what are apthous ulcers?

Back 267

-small painful shallow ulcers of the oral cavity
-triggered by stress, fever, or certain foods and are mainly in children/young adults

Front 268

almost all oral cancers are...

Back 268

squamous cell carcinomas

Front 269

what is a pleomorphic adenoma?

Back 269

-tumor of the salivary gland
-often called a 'mixed tumor' b/c of varied microscopic appearance
-almost all are benign, but can be trouble because branches of the facial nerve pass thru the parotid so can be difficult to excise and function may be lost of this portion of the nerve

Front 270

Mallory-Weiss syndrome

Back 270

-severe retching can cause esophogeal laceration
(as in bulimia)
-occur at GE junction, can be life threatening bleeding

Front 271

peptic ulcers

Back 271

-usually found in duodenum
-also are in stomach & esophagus
- infection by H. pylori is necessary
but other factors can be involved.
-can come from cigarette use etc. more men than women
-80% are in first few cm of duodenum.
-ulcer floor is a bed o granulation tissue and inflammatory debris, surrounded by rim of inflamed edematous mucosa

Front 272

Zollinger-Ellison syndrome

Back 272

-pancreatic islet tumors secrete gastrin, which stimulates marked gastric acid production & recurrent ulcers that resist medical tx.
-surgical removal required

Front 273

what are the most prevalent malignancies of stomach?

Back 273

95% are from adenocarcinomas
also, is 10x more common in Japan

Front 274

what are some risks of gastric carcinoma?

Back 274

1-H. pylori infection
2- diet high in pickled, smoked or salt-preserved food
3- use of nitrite food preservatives
4- diet low in fresh fruit & vegetables

Front 275

Meckel diverticulum

Back 275

-the most common and harmless bowel congenital anomaly
-embryologic remnant attached to the jejunum like large appendix
-rarely becomes inflamed like appendix

Front 276

what is gastroschisis?

Back 276

-failure of abdominal wall to form properly
-as a result intestines are uncovered & protrude outward
-less severe form is an ompalocele
-smaller is umbillical hernia

Front 277

angiodyslplasia

Back 277

a small tortuous collection of small blood vessels (somewhat like a hemangioma)
-usually found in mucosa/submucosa of right colon or cecum
-prone to bleed, account for 20% of lower intestinal bleeding, esp in older adults

Front 278

what is dysentery

Back 278

-low volume, bloody painful diarrhea

Front 279

enterocolitis

Back 279

inflammation of the bowel assoc with diarrhea, almost always infectious
-happens in one of 2 settings;
-->1 equilibrium of intestinal flora is upset and normal bactera overgrows (C. diff diarrhea)
-->2 pathogen like rotavirus, Giardia, Salmonella is introduced

Front 280

bacterial enterocolitis

Back 280

-usually more severe than viral, produced by one of the 2 main mechanisms,
-diagnosis confirmed by stool culture of organism

Front 281

typhoid fever

Back 281

-less common
-syndrome of slow onset of GI and systemic symptoms including:
-fever, HA, sore throat, splenomegaly, bloating, constipation, diarrhea, skin rash

Front 282

pseudomembranous colitis

Back 282

>uncommon, severe inflamation of coloinc mucosa usually seen in elderly
>caused by enterotoxin by C. diff.
-dx: by stool culture

Front 283

hereditary nonpolyposis colerectal carcinoma syndrome

Back 283

> a rare genetic disorder that deserves mention b/c it is the sole exception to the rule that all colon cancers arise from preexisting polyps

Front 284

Astler-Coller Staging

Back 284

side note: most important prognostic factor in colorectal carcinoma is the clinical stage of the neoplasm at the time of dx.
>AC staging most widely accepted
>relies on assmnt of depth of bowel wall invasion by the tumor, presence or absense of lymph nodes metastasis, & clinical assmnt of distant mets to liver/other organs

Front 285

CEA (carcinoembryonic antigen)

Back 285

>not good for screening for colon cancer (b/c secreted by other tumors)
>it is a useful monitoring tool to check for tumor regression/recurrence after acute therapy

Front 286

how does blood flow through the liver?

Back 286

1-venous blood flows from intestinal veins up the portal vein,
2-which divides into progressively smaller vessels to form a secondary capillary network in the liver
3-from there blood flows into hepatic vein & then
4-inferior vena cava/systemic circ.
5-arterial blood flows thru 2nd set of capillaries that branch from the hepatic artery
-then mixes w/ portal blood to flow thru hepatic vein & into vena cava

Front 287

major functions of the liver

Back 287

1-clears blood of toxins, metabolic waste, hormones
2-converts glucose/glycogen for energy storage & reconverts it to glucose on demand
3-produces most plasma proteins w/ the exception of antibodies
4-excretes bilirubin into bile
5-produces bile acids & excretes them into bile

Front 288

explain the enterohepatic circulation

Back 288

>it refers to the excretion of bile acids from the liver into the intestine & the reabsorption of most of the bile acids by the intestine for recirculation thru the portal system & reuse by the liver.
>most cholesterol in the body comes from bile acids not diet.

Front 289

major functional reactions of liver to injury

Back 289

>jaundice
>cholestasis
>hepatic failure

Front 290

unconjugated bilirubin

Back 290

>is not water soluble, attached to albumin for transport to the liver

Front 291

conjugated bilirubin

Back 291

>joined to glucuronide & becomes H20 soluble & excreted as bile by the liver

Front 292

unconjugated bilirubinemia

Back 292

>can occur with hemolytic anemia
(sickle cell disease)
>can cause incr production of unconjugated bilirubin

Front 293

conjugated bilirubinemia

Back 293

occurs when bile flow is obstructed after bilirubin has been conjugated by the liver,
(bile duct obstruction)

Front 294

what is cirrhosis,
what are 2 most common causes?

Back 294

>is a progressive patterned fibrosis of entire liver
ex: alcoholism & chronic hepatitis

Front 295

why does cirrhosis cause portal hypertension?

Back 295

>when there is obstruction of portal blood flow caused by the choking action of the dense fibrous bands of cirrhosis, which scar & shrink the liver

Front 296

what are 2 hemodynamic consequences of portal hypertension?

Back 296

>the hemodynamic consequences of portal HTN:
-->ascites, congestive splenomegaly, esophogeal varices, hemorrhoids, & radiating prominent preumbilical veins (caput medusa)

Front 297

what are the main clinical manifestations of cirrhosis in general ?

Back 297

1-portal HTN causes hemorrhoids, esophogeal varices, splenomegaly, & caput medusa veins from umbillicus
2-failing hepatic metabolism of estrogen results in high blood levels of it.
3- ammonia metabolism affected leads to hepatic coma & fetor hepaticus
4- failed bilirubin excretion = jaundice
5-failing protein synthesis cause decr in plasma albumin -->ascites/edema
6-low blood coagulation factors -->bleeding tendancies, evident w/ easy bruising

Front 298

what are the main clinical manifestations of cirrhosis in and in men/women?

Back 298

women >may have abnormal menstrual bleeding,
men> to thinning hair (head/genital), bitch tits, red palms, atrophic testes, spider angiomas

Front 299

what are some clinicopathologic syndromes associated with viral hepatitis?

Back 299

-asymptomatic hepatitis
-carrier state
-acute viral hepatitis
-chronic viral hepatitis
-fulminant viral hepatitis
-hepatocellular carinoma

Front 300

mode & transmission of hepatitis A

Back 300

HAV: transmitted by personal contact, oral-fecal contamination of food/water
->benign, self-limited, with no carrier state, no chronic hepatitis

Front 301

mode & transmission of hepatitis B

Back 301

HBV->contracted by injection of blood products,renal dialysis, needle stick accidents, IV drug use,
sex,
->more serious, may cause sypmtomatic acute hepatitis, fulminant hepatitis, w/ massive liver necrosis, OR chronic necrosis that may advance to cirrhosis (small percentage become carriers)

Front 302

what is the most important epidem. fact about Hep C and other facts?

Back 302

Hep C: consequence of IV drug abuse
>high rate of progression to chronic hepatitis and cirrhosis

Front 303

what is one acute & one common chronic change in the liver induced by alcohol abuse?

Back 303

>most common change is fatty metamorphosis (steatosis), the most common serious chronic change is cirrhosis

Front 304

primary biliary cirrhosis

Back 304

-is an autoimmune disease of intrahepatic bile ducts
-most pts have other autoimmune disease & anti mitochondrial antibody in their blood

Front 305

primary sclerosing cholangitis

Back 305

>is a chronic inflammatory disease of intrahepatic & extrahepatic bile ducts usually associated w/ ulcerative colitis

Front 306

what is the liver condition commonly assoc. w/ hepatocellular carcinoma?

Back 306

> chronic hepatitis, caused by Hep B or C infexn.

Front 307

what are 2 kinds of gall stones?
which is more common?

Back 307

>cholesterol stones (most common)
> pigmented stones

Front 308

what are several risk factors that favor the formation of gallstones?

Back 308

age, gender, ethnicity,
>old more than young
>women more tha nmen
>native americans/hispanics more than anglos
>oral contraceptives, ERT,
obesity, hemolytic anemia & rapid wt loss

Front 309

what are some of the most common causes of extra hepatic bile duct obstruction?

Back 309

>gallstones are the most common cause of extrahepatic biliary obstruction
> other causes include biliary atresia in newborn infants, cancer of the head of the pancreas, pancreatitis, inflammatory disease of the ducts, and postop scarring
>serious complication: ascending cholangitis (bacterial infection that enters the biliary tree from the intestine)

Front 310

what are Councilman bodies?

Back 310

>shrunken dead cells of the liver

Front 311

how are hepatitis viruses distinguished from one another?

Back 311

-mode of transmission
-length of incubation period
-carrier state
-chronic hepatitis
-fulminant hepatitis
-hepatocellular carcinoma

Front 312

hemachromatosis

Back 312

>iron overload, toxic accumulation of an excessive amount of iron in cells esp in liver(heart & pancreas)
>primary: inherited, autosomal recessive. one of most common inborn errors of metabolism in US
>secondary: acquired, usually result of repeated blood transfusions given as tx for sickle cell anemia, thalassemia, aplastic anemia

Front 313

HBV : more facts

Back 313

>transmitted: blood, saliva, semen
sex
>carrier state evolves in <10%
>in blood: hepatitis B surface antigen (indicates acute infxn)
>HBV antigens appear first, then HBsAg first marker to appear, indicates viremia/infectivity
>hepatitis core antigen: first to appear, early indicator of fnx
>anti HBs-marks beginning of recovery, confirm immunity

Front 314

HAV: more facts

Back 314

>epidemic, food borne
>most people in developed countries have anti-HAV antibodies
>clinical markers of disease process: incr liver enzymes, appearance of IgM type anti HAV antibodies (note IgM are actue phase antibodies)

Front 315

HCV: more facts

Back 315

>viremia: marked by detection in blood of virus RNA (HCV-RNA)
-acute infection: anti HCV appears promptly as marker of acute immune respnose but does NOT confer immunity
25-35% develop cirrhosis
>many have relapsing symptoms

Front 316

how much alcohol is necessary to produce cirrhosis?

Back 316

200 grams ethanol per day
(one pint of whiskey etc)
for 10-16 years

Front 317

Wilson's disease

Back 317

-incredibly rare autosomal recessive disorder of Copper metabolism
-confirmed by liver biopsy, copper deposits in the eye can occur, early diagonsis is critical
-liver transplant is only permanent cure

Front 318

autoimmune hepatitis

Back 318

-20% of all cases of chronic hepatitis, syndrome of chronic hepatitis
-mild to severe
-no blood markers of viral hepatitis are present, but a few pts with false positives
-many pts have high levels of autoantibodies: ex: ulcerative colitis, Sjogren, SLRE, thyroiditis
-increased frequency of association with certain HLA genotypes

Front 319

liver abscess

Back 319

-focal collection of necrotic and acute inflammatory debris & fluid
-most often caused by bacteria or fungi
-occurs most often in immunodeficient, tx with abx and surgery in advanced cases
-developing world: caused by Entamoeba histolytica (protozoan)

Front 320

fatty liver

Back 320

-alcoholics develop this
-usually asymptomatic, mild elevations of LE's
-dying hepatocytes appear as small, round, dark cells (Councilmain bodies) & Mallory's alcoholic hyaline

Front 321

hepatocellular carcinoma

Back 321

-malignant neoplasm
-related to chronic hepatitis from Hep B and C
-high incidence in Africa/Asia
-grows as a single massive neoplasm
-most pts have increased level of alpha fetoprotein in their blood, but it isn't a specific marker (can also be seen in cirrhosis) but if really high can't be anything else
-prognosis is bad

Front 322

most common benign tumor of the liver is?

Back 322

cavernous hemangioma
-small, located beneath fibrous capsule of liver

Front 323

cholangiocarcinoma

Back 323

malignancy of bile duct epithelium
-most arise w/out preexisting risk factors
2 known associated conditions:
-primary sclerosing cholangitis
-chronic liver infection with shistomiasis

Front 324

cholelithiasis

Back 324

-gall stones, most form in the GB
-some form in the bile ducts
-80% are cholesterol stones
--female, fat, forty, family, (indian,hopi) oral contraceptives
20% are pigment stones
--biggest risk factor is sickle cell anemia

Front 325

cholecystitis

Back 325

-acute cholecystitis is most common complication of gallstones, from obstruction of neck of GB by stone
-can occur without stones though.
-most cases are nonbacterial

Front 326

ascending cholangitis

Back 326

-when bacteria from gut ascend into common bile duct cause problems (happens more in asia)
-in US most common cause of obstruction are stones

Front 327

biliary atresia

Back 327

obstruction of extrahepatic bile ducts discussed in conjuction with neonatal cholestasis
-cause unknown, reason for over half of liver txplnts in children

Front 328

describe the anatomy of the pancreas

Back 328

-tadpole shaped organ, 5-6 inches long, embedded in retroperitoneal fat in mid abdomen lying across the front of the aorta.

Front 329

distinguish between the digestive and hormonal pancreas

Back 329

digestive pancreas: composed of acini & ducts.
ducts lead from individual pancreatic glands (acini) and join to form the pancreatic duct, which empties into the duodenum. Epithelial cells of the acini excrete digestive enzymes into the ductal system, which empties into duodenum.
-Hormonal pancreas: composed of many tiny islets of Langerhans scattered throughout the gland. not connected to ductal system, and secrete hormones directly into the blood

Front 330

explain the relationship of glucose, glucagon, and insulin to one another and stored glycogen

Back 330

-level of blood glucose is controlled by the opposing effects of insulin & glucagon
-insulin acts on muscle & other cell membranes to allow glucose to enter cells to be burned for energy production
-constant balance between blood sugar & insulin
-high blood glucose --> insulin
-low blood glucose -->glucagon

Front 331

2 most common causes of acute pancreatitis

Back 331

-gallstones
-alcohol abuse

Front 332

autodigestion in acute pancreatitis

Back 332

`pancreatic enzymes are normally excretd in the inactive form,
-in pancreatitis they are liberated from the ducts, activated prematurely, and begin the digestive process while still in the cell or in the pancreas
-->pancreas digests itself & release additional activated enzymes in a vicious circle

Front 333

why would a pt with acute hemorrhagic pancreatitis develop hypovolemic shock and/or hypocalcemia?

Back 333

-acute hemorrhagic pancreatitis causes massive edema & pooling of blood & fluid in and around the pancreas.
-hypocalcemia may occur as calcium soaps are precipitated in ares of pancreatic fat necrosis

Front 334

acute pancreatitis

Back 334

-sudden and painful, can be catastrophic medical emergency
assoc w/ shock/death
->systemic organ failure: ((shock/acute respiratory distress syndrome (ARDS/acute renal failure))
->disseminated intravascular coagulation
->pancreatic pseudocyst
->duodenal obstruction

Front 335

chronic pancreatitis

Back 335

occurs following repeated episodes of acute pancreatitis
-less dramatic, less painful, less dangerous
-associated with pancreatic fibrosis, ductal stone formation, and pancreatic calcification
-complications- migratory thrombophlebitis and malabsorption syndrome
->pancreatic pseudocyst
->common bile duct obstruction
->intestinal malabsorption
->secondary DM

Front 336

what is the most common cause of acute pancreatitis?

Back 336

alcohol abuse

Front 337

status asthmaticus

Back 337

potentially fatal, severe asthmatic bronchospasm
-bronchioles become plugged with thick, sticky mucus that obstructs airflow into and out of the alveoli (gas exchange stop)
-dire emergency; pts become cyanotic from retained CO2

Front 338

adenocarcinoma of pancreas
CP, prognosis

Back 338

-presents as upper abdominal pain or back pain first sytm
-painless jaundice may be initial sign if tumor obstructs the common bile duct
-unexplained wt loss, migratory thrombophlebitis should always suggest a hidden malignancy (esp. pancreatic cancer)
-only 1% of pts w/ pancreatic carcinoma survive 5 years

Front 339

explain pathogenesis of type 1 DM

Back 339

type 1 DM: autoimmune disease that destroys islets of Langerhans & their ability to produce insulin

Front 340

explain the pathogeneis of type 2 DM

Back 340

-caused by peripheral resistance to insulin
-which makes the pancreas produce more insulin,
-associated with obesity, pregnancy, steroid excess, other contitions.
-later in DM2, pancreatic insulin production falls and beta cells wear out from insulin overproduction

Front 341

what are the 2 most important factors that lead to development of type 2 DM?

Back 341

obesity - 80% of type 2 DM pts are obese

Front 342

name 2 types of diabetic coma & pathogenesis of each

Back 342

-can occur from: acidosis, OR severe dehydration
-acidosis occurs when insulin is lacking: when glucose is unavailable the body burns fat --ketone bodies are acidic-- which can lead to coma
>coma of severe dehydration occurs in pts with severe prolonged glycosuria, which wastes water & electrolytes
-urine containing large amts of glucose has high osmotic pressure which attracts water so urine output rises & coma can occur from dehydration

Front 343

explain the pathogeneis of type 2 DM

Back 343

-caused by peripheral resistance to insulin
-which makes the pancreas produce more insulin,
-associated with obesity, pregnancy, steroid excess, other contitions.
-later in DM2, pancreatic insulin production falls and beta cells wear out from insulin overproduction

Front 344

explain the importance in DM of hyperglycemia and glycosylation

Back 344

-high blood glucose levels are the cause of all diabetic complications
-hyperglycemia causes abn attachment of glucose to protein molecules (glycosylation)
-abnormal molecules acceleate atherosclerosis & are the major cause of diabetic microvascular disease

Front 345

what are the 2 most important factors that lead to development of type 2 DM?

Back 345

obesity - 80% of type 2 DM pts are obese

Front 346

name 2 types of diabetic coma & pathogenesis of each

Back 346

-can occur from: acidosis, OR severe dehydration
-acidosis occurs when insulin is lacking: when glucose is unavailable the body burns fat --ketone bodies are acidic-- which can lead to coma
>coma of severe dehydration occurs in pts with severe prolonged glycosuria, which wastes water & electrolytes
-urine containing large amts of glucose has high osmotic pressure which attracts water so urine output rises & coma can occur from dehydration

Front 347

explain diabetic microvascular disease

Back 347

diabetic microvascular disease is a condition of capillaries & other small vessels damaged by high blood glucose levels
--slows blood flow & diffusion of critical substances into tissues
-it is major pathologic mechanism of diabetic retinal disease & diabetic kidney disease

Front 348

explain the importance in DM of hyperglycemia and glycosylation

Back 348

-high blood glucose levels are the cause of all diabetic complications
-hyperglycemia causes abn attachment of glucose to protein molecules (glycosylation)
-abnormal molecules acceleate atherosclerosis & are the major cause of diabetic microvascular disease

Front 349

explain diabetic microvascular disease

Back 349

diabetic microvascular disease is a condition of capillaries & other small vessels damaged by high blood glucose levels
--slows blood flow & diffusion of critical substances into tissues
-it is major pathologic mechanism of diabetic retinal disease & diabetic kidney disease

Front 350

leading causes of death in DM

Back 350

MI
kidney failure
stroke

Front 351

name criteria for diagnosis of DM

Back 351

classic S&S:
-polyuria, polyphagia,polydipsia, wt loss
-any random blood glucose level equal to or greater than 200 mg/dL
-fasting blood glucose level equal or greater than 126 mg/dL
-after OGTT test 2-hour postprandial blood glucose equal to or greater than 200 mg/dL

Front 352

the hormonal pancreas (endocrine)
(the different types of cells)

Back 352

Alpha Cells - secrete glucagon (fasting hormone) turns glycogen into glucose
Beta Cells - secrete insulin (turn glucose into glycogen among other things)
Delta Cells - somatostatin (inhibits secretion of aforementioned two, slows peristatlsis in GI system)

Front 353

annular pancreas

Back 353

congenital deformity in which the head of pancreas encircles the duodenum & may cause duodenal obstruction

Front 354

ectopic pancreas

Back 354

embryologically misplaced but histologically normal pancreas that has come to rest in an abnormal place
(the 'rests' occur in 2% of people)
occur in submucosa of stomach & bowel and are rarely symptomatic

Front 355

other conditions associated with acute pancreatitis

Back 355

-Gallstones (half of pts with pancreatitis have them, will get more attacks if they aren't taken out)
-Alcoholism: 2/3 assoc with
-Unknown - 10% idiopathic
-Other - virus, blunt trauma, thiazide diuretics, high serum TG's and calcium.

Front 356

acute hemorrhagic pancreatitis

(pseudocyst included)

Back 356

inflamed bleeding pancreatitis
-entire pancreas can be destroyed
-common outcome if you survive is a formation of a cyst by fibrous 'walling off' of inflammatory fluid
-->can be come a pancreatic pseudocyst

Front 357

typical presentation of acute pancreatitis

Back 357

-severe abdominal pain radiating to back
-rapid progression
-renal failure and Respiratory distress syndrome
-bloody mass of necrotic tissue becomes infected in many pts

Front 358

acute hemorrhagic pancreatitis

Back 358

-medical emergency
-need lab tests to confirm
-need to differentiate it from perforated duodenal ulcer
--ALL acute pancreatitis is hypothetically reverisible

Front 359

chronic pancreatitis- elaborated

Back 359

-has distinctly different clinical presentation
-half of pts have evidence of prior episodes of acute pancreatitis
-others have obscure sx with abd pain radiating to back but nonspecific
-pancreas is choked with scars

Front 360

carcinoma of the pancreas

Back 360

-arise in the digestive pancreas (exocrine)
-are dense scar-filled tumors, arise in head of pancreas mostly, cause jaundice by obstructing common bile duct
-LOCAL lymph nodes & liver are the foremost sites of metastasis
-upper abd/back pain first sx
-unexplained wt loss. migratory thrombophlebitis

Front 361

diabetic ketoacidosis
is characterized by:

Back 361

->rapid deep breathing (Kusmals)
->glycosuria
->acidosis
->ketonuria
->osmotic diuresis
->volume depletion
-->can lead to a diabetic coma, often more associated with type 1 than type 2 (because glucose metabolism in type 1 is more unstable or BRITTLE)

Front 362

hyperosmolar coma

Back 362

-second type of diabetic coma
-can occur if water loss is especially severe
-and blood glucose levels are extremely high

Front 363

long term complications of DM

Back 363

-accelerated atherosclerosis
-MI
-stroke
-PVD (periph vascular)
-renal insufficiencyd
-peripheral nerve disease
-infections are common, possibly due to def. immune response

Front 364

hyaline arteriosclerosis

Back 364

-microscopically distinctive changes in small blood vessels
-kidney and retina most severely damaged
-->changes in kidney/retina are called diabetic nephropathy/reinopathy respectively

Front 365

other stuff common in diabetics

Back 365

-diabetic nephrosclerosis
-cystitis
-pyelonephritis
(kidneys are small and shrunken in the diabetic)
-also cataracts, glaucoma, optic nerve damage
-peripheral neuropathy --sensoral functions affected more, esp in lower limbs,
-postural hypotension
-erectile dysfunction & bladder control problems

Front 366

insulinomas (beta cell tumors)

Back 366

-usually occuring as a single small benign tumor mass in pancreas
-secretes enough insulin to produce HYPOGLYCEMIA

Front 367

Zollinger-Eillison syndrome

Back 367

constellation syndrome
-gastrinomas (arise in stomach, pancreas, duodenum)
-produce large amounts of gastrin
-incr gastric acid production
-ulcers identical to precipitators of H. pylori infection

Front 368

glucagonoma

Back 368

-tumor of alpha cells
-exceptionally rare & causes, skin disease, and anemia

Front 369

what are homeostatic feedback loops?

Back 369

-self adjusting forces that operate to oppose movement of any physiologic function away from its healthy range
-ex: if thyroid hormone goes too high or too low the pituitary acts to return it. same with pancreas and insulin/glucagon.
-physiology = feedback loops
(body temp, pH, blood pressure etc)

Front 370

example of change in blood hormone levels in an endocrine disease & how feeback is involved

Back 370

-sometimes the feedback doesn't work
-thryoid disease: the thyroid escapes pituitary control & goes rogue, secretes massive amounts of thyroid hormone (hyperthyroidism)
-high levels of thyroxine cause pituitary to produce LOWER amounts of thyroid stimulating hormone in effort to lower blood thyroid hormone levels.
-but because thyroid is operating independently, blood levels of thyroid hormone remain high & blood levels of TSH remain low in some kinds of hyperthyroidism

Front 371

mass effect in pituitary disease

Back 371

-result of pressure exerted by a pituitary mass on the remaining normal pituitary gland tissue and on nearby structures
ex: tumor may press on optic nerves to produce visual problems

Front 372

stalk effect in pituitary disease

Back 372

effect of a pituitary mass on the stalk that induces secretion of abnormal amounts of prolactin by the pituitary gland

Front 373

what is the most common type of functioning pituitary adenoma

Back 373

prolactinoma

Front 374

acromegaly

Back 374

-occurs when abnormal secretion of growth hormone occurs in adults after bone growth plates disappear and epiphyses close. patients have large hands and feet & other distinctive features but are not otherwise exceptionally large or tall

Front 375

gigantism

Back 375

>occurs when abnormal growth hormone secretion occurs before closure of bone epiphyseal growth plates & is characterized by generalized increase of body size with disproportionately long arms & legs

Front 376

thyroglobulin

Back 376

a globulin protein in the thyroid gland that binds to thyroid hormones while they are stored in the gland
-releases thyroid hormones into blood

Front 377

thyroxin binding globulin

Back 377

-a globulin in blood to which thyroid hormones are attached
-TBG transports thyroid hormones from the thyroid gland to target tissues

Front 378

define: goiter

Back 378

a goiter is an enlarged thyroid gland

Front 379

why are TSH levels decreased in Graves disease?
(and other forms of primary hyperthyroidism)

Back 379

in primary hyperthyroidism the gland itself is diseased
-->the gland produces too much hormone
TSH is low

Front 380

why are TSH levels increased in primary hypothyroidism?

Back 380

in primary hypothyroidism the gland itself is diseased
-->the gland does not produce enough hormone
TSH is high

Front 381

what is the most common type of thyroiditis?
pathogenesis?

Back 381

Hashimoto thyroiditis
-is a chronic autoimmune disease

Front 382

what is the most common type of thyroid cancer?
-5 year survival figure?

Back 382

papillary carcinoma,
about 90% survive after 5 years

Front 383

what are the lab abnormalities in hyperparathyroidism?

Back 383

-blood levels of calcium and parathormone are high
blood levels of phosphate are low

Front 384

what are the important hormones produced by the adrenal medulla?

Back 384

-epinephrine
-norepinephrine

Front 385

what are the important hormones produced by the adrenal cortex?

Back 385

-cortisol (hydrocortisone)
-aldosterone
-androgenic steroids

Front 386

what is the adrenocortical hormone for most of the clinical features of Cushing syndrome?

Back 386

-Cortisol (hydrocortisone)
or excess amounts of it

Front 387

what is the most common cause of Cushing syndrome?

Back 387

steroid drug therapy

Front 388

why do patients with HTN caused by primary hyperaldosteronism have low blood levels of renin?

Back 388

-high blood aldosterone suppresses renal secretion of renin

Front 389

why do patients with Addison disease have dark skin?

Back 389

low blood levels of cortisol causes the pituitary gland to secrete large amounts of ACTH
-one of the metabolic breakdown products of ACTH is melanocyte stimulating hormone (MSH) which then stimulates melanin production in the skin

Front 390

why do pts with pheochromocytoma have high blood pressure?

Back 390

-pheochromocytomas secrete large amounts of epinephrine and norepinephrine (catecholamines) both of which cause peirpheral vasoconstriction, which then causes increased vascular resistance and increased blood pressure

Front 391

what are the nonendocrine organs and tissues?

Back 391

-uterus, breast, kidney bone and muscle
DO NOT HAVE A NEGATIVE FEEDBACK LOOP

Front 392

what are the organs that have endocrine activity?

Back 392

adrenal glands
thyroid gland
ovary
testis
(release their own hormones for final effect)
-interact with pituitary in a negative feedback loop

Front 393

how does PTH control calcium homeostasis ?

Back 393

-controls calcium with a negative feedback loop
-activates osteoclasts to release calcium into blood
-increase Ca abs in gut
-incr renal retention of Ca
-incr urinary phosphate excretion
-activating vitamin D

Front 394

what is the role of cortisol?

Back 394

-increase glucose production (by muscle catalysis)
-breaking down fat into FFA's
-inhibits peripheral glucose utilization to save it for the brain
-supresses immune reaction and limits inflammation to lessen the stress of injury/disease

Front 395

what does aldosterone do?

Back 395

acts on kidney to retain sodium and water
and excrete potassium (both increase blood volume and pressure)

Front 396

which affects more, the anterior or posterior pituitary?

Back 396

-the posterior is extension of the brain and regulates water retention by the kidney
-the anterior has its hands it way more pies that are discussed on another card

Front 397

roles of the anterior pituitary?

Back 397

-controls function of thyroid and adrenal glands, sperm and ovum production, bone and soft tissue growth, and breast milk formation
-if pituitary is affected by any disease it's always the anterior pituitary that is in the middle of it.

Front 398

what is a functioning adenoma?

Back 398

a benign hormone secreting tumor
-formed from one of the cell types that the anterior pituitary is made of
NOTE: it is the most common anterior pituitary mass (is an adenoma)

Front 399

2 consequences of masses in the pituitary gland (other than making hormones)

Back 399

1-mass effect:
2-stalk effect

Front 400

what is a prolactinoma?

Back 400

a benign tumor of anterior pituitary that secretes prolactin
-stimulates mlik production
-most COMMON functioning pituitary tumor
-causes amenorrhea, milk production and infertility/loss of sex drive in women

Front 401

what is a growth hormone (somatotropin) adenoma?

Back 401

-2nd most common functioning adenoma of the ant. pituitary
-many secrete prolactin as well
-leads to gigantism and acromegaly

Front 402

ACTH adenoma

Back 402

-adenoma of ant pit. that secretes adrenocorticotropin. accounts for 15% of pitry. adenomas.
-causes excessive secretion of cortisol... produce Cushing Syndrome

Front 403

luteinizing hormone adenoma/follicle stimulating hormone adenomas

Back 403

-10% of AP adenomas
-very low hormone effect
-usually noticed b/c of mass effect
(most common in middle age women/men)

Front 404

thyroid stimulating hormone adenoma

Back 404

-rarest ~1%
-produces symptoms similar to overactive thyroid gland

Front 405

null cell carcinoma

Back 405

-occurs as often as prolactinomas
(which is also the most common functioning pituitary tumor)
-only comes to attention when it produces the stalk effect that stimulates the remaining normal pituitary to secrete prolactin or b/c it destroys the rest of the gland by mass & causes pituitary failure

Front 406

how much pituitary has to be ruined before you have failure of the gland?

Back 406

75% of anterior pit. must be destroyed for hormonal deficit to become symptomatic

Front 407

what are the most common causes of pituitary failure?

Back 407

in order:
1-mass effect
2-pituitary destruction caused by vascular ischemia with necrosis (pituitary infarction)
3-surgical/radiotherapeutic destruction

Front 408

what is Sheehan syndrome?

Back 408

infarction of the pituitary in pregnacy.
--when the pituitary enlarges b/c of prolactin producing cells the blood supply doesn't catch up --infarction ensues.
-can cause hemorrhage/shock
-suspect in a woman who doesn't resume normal menstrual periods after delivery/sx of thyroid failure

Front 409

posterior pituitary... basics

Back 409

part of the brain. its hormones are made by the hypothalamus and sent down
-ADH and oxytocin

Front 410

what does ADH do?

Back 410

acts on renal tubules to stimulate retention of water
-deficiency of it causes DIABETES INSIPIDUS (very hi output of dilute urine) --> dehydration

Front 411

what is oxytocin?

Back 411

-posterior pituitary
-stimulates uterine smooth muscle contractions in labor, breast duct smooth muscle contraction in milk
-no clinical syndromes of oxytocin abnormality

Front 412

Causes of hyperthyroidism

Back 412

-overmedication with T3-T4 in treatment of thyroid gland failure
-increased thyroid gland output of hormone associated with disease of the thyroid gland (primary hyperthyroidism)
-increased thyroid gland output of thyroid hormone caused by TSH by ant. pit. (2ndary hyperthyroidism)

Front 413

Graves disease

Back 413

accounts for 80-90% of all hyperthyroidism
-characterised by:
(of course) hyperthyroidism
-enlarged thyroid gland (goiter)
-exophthalmos
-minority of pts have weird skin over shins

Front 414

what is one of the most common autoimmune diseases in US?

Back 414

Graves disease
(young women, often with other autoimmune disease)
-they have Thyroid-stimulating immunoglobulin in their blood
-weird shin skin thing(pretibial myxedema) isn't as common but bugged eyes is .(because of fat deposition behind the eyeballs)
--pretib myxedema not to be confused with general myxedema. they're not the same

Front 415

clinical presentation of Graves disease

Back 415

-weight loss, sweating, heat intolerance, increased appetite,bowel hypermotility (can lead to malabsorption)
-nervousness, irritability, tremor, rapid HR, palpitations, exophthalmos
-lid lag, blood levels of T3-4 are increased

Front 416

radioactive iodine uptake

Back 416

-useful tool in dx of thyroid dz
-pts given small dose of radioactive iodine
-overactive glands take up an abnormally large amount of the administered dose.

Front 417

myxedema

Back 417

baggy eyes, swollen tongue
edema of the vocal cords & hoarseness, swelling of the hands & feet, pleural & pericardial effusions, wt gain
hair loss is common

Front 418

cretinism

Back 418

infantile or early childhood hypothyroidism, is a cause of short stature & mental retardation

Front 419

goiter

Back 419

most common thyroid abnormality
big ole thing on your neck because your thyroid gets so huge from
-not associated with abnormal function
-may be assoc w/ hyper or hypo thyroidsm
-gets big because of iodine deficiency: TSH continuously stimulates it

Front 420

thyroiditis

Back 420

inflammation of thyroid gland
-most is chronic (b/c of thyroid autoimmunity)
-may or may not be hypothyroid, may have gland tenderness

Front 421

Hashimoto thyroiditis

Back 421

-most COMMON type of thyroiditis in US.
-chronic autoimmune disease
-accumulation of lymphoctyes in gland
-half of first degree relatives have antithyroid antibodies or some other type of autoimmune disease (middle aged women (90% of cases) most have normal thyroid function, unless it gets destroyed and then they don't.

Front 422

Subacute (granulomatous) thyroiditis

Back 422

much less common than Hashimoto's
-more in women than men
-tender, painful swallowing, fever, malaise, high white blood cells.
self limiting, resolves in 6-8 wks.

Front 423

neat facts about thyroid masses

Back 423

-less than 1% are malignant
-all must be checked out
-solitary ones are more likely than multiple ones to be neoplastic
-masses that are 'cold' (do not take up radioactive iodine) are more likely than 'hot' to be neoplastic
-masses in young are more likely to be neoplastic than those of old
-masses in males are more likely to be neoplastic (than female)

Front 424

thyroid adenomas

Back 424

benign neoplasms of the epithelial cells that line the thyroid follicles
-painless pass, normal woman
-are 'cold' do not develop into carcinoma

Front 425

papillary carcinomas

Back 425

80% of thyroid cancers, in women mostly
-grow really slow, most pts survive
-cauliflower like microscopic growth pattern
-TENDANCY FOR LYMPHATIC INVASION/METS
(whereas tumors of endocrine tend toward vascular invasion)

Front 426

follicular carcinoma

Back 426

characterized by the production of follicles, no papillary growth is present
-15% of thyroid cancers
-older age group
-much more likely to spread to blood, lungs, bone liver. most tx is surgical excision

Front 427

what are the 3 kinds of hyperparathyroidism?

Back 427

primary - caused by parathyroid hyperplasia/adenoma
secondary -
tertiary - both 2ndary/3 are due to chronic renal failure
-all feature overactivity of these glands.

Front 428

what is the second most common endocrine disorder

Back 428

-second to diabetes mellitus
---primary hyperparathyroidism
-CP: stones, bones, groans/ moans/ groans - peptic ulcers
moans- depression
(stones kidney, bones deossify)
MOST ARE ASYMPTOMATIC
lab value: high pth and calcium

Front 429

how does chronic renal failure and 2ndary hyperparathyroidism work?

Back 429

CRF is assoc with high blood phosphate levels, which pushes blood calcium levels down, causes parathyroids to secrete increased amts of PTH to raise blood calcium which then causes parathyroid cells to proliferate to make more PTH
-when this won't go awawy becomes TERTIARY hptism.

Front 430

major blood abnormality associated with underactive thyroid glands is...

Back 430

low blood calcium levels
-causes tetany
-tingling, muscle spasms, seizures, vocal cord spasm, airway obstruction
tx;CALCIUM & VITMIN D

Front 431

Cushings syndrome

Back 431

excessive blood cortisol
causes:
-anterior pituitary hyperplasia/tumor
making too much ACTH
-secretion of ACTH by nonendocrine tumors (like small cell carcinomas of the LUNG)
-adrenal cortex hyperplasia/tumor assoc with excessive secretion of corticosteroids in blood
-overmeidcation with steroids

Front 432

adrenocortical adenoma

Back 432

occurs as single nodule in one adrenal gland
-very rare

Front 433

hyperaldosteronism

Back 433

-excessive aldosterone, leads to high BP, low K, low blood renin
-can be caused by adrenocortical disease (primary/Conn syndrome) which is overgrowth/hyperplasia

or secondary: impaired renal blood flow 2ndary to renal artery stenosis, invokes the RAAS

Front 434

congential adrean hyperplasia

Back 434

-adrenogential syndrome
-genetic defect results in enzyme deficiencies in adrenal cortex
-boil down to 2 problems:
-incr in androgenic steroids
-decrease of aldosterone/cortisol
-female infants with 'ambiguous' genitals (she has a penis)
-males usually diagnosed later (precocious puberty)
-can result in salt wasting syndrome

Front 435

adrenocortical insufficiency

Back 435

-lack of adrenocortical hormones, esp cortisol
-almost every condition affecting adrenals affects both glands
-can be caused by adrenal pland (primary) or pituitary gland disease (secondary failure)

Front 436

acute adrenocortical crisis

Back 436

-acute adrenal failure occurs in 3 clinical settings (are fatal without quick dx and tx)
--sudden withdrawl of corticosteroid tx (these drugs atrophy the adrenal cortex, if withdrawn quickly they have none and die)
--bilateral acute hemorrhagic infx of adrenal glands (in meningococcal meningitis)
--sudden worsening of chronic adrenal insufficiency

Front 437

Addison disease

Back 437

-chronic adrenocortical insufficiency
-fatal without corticosteroid replacement
-most cases (60-70%) are from autoimmune dz
-also from TB or fungus
-physiologically fragile, darkening skin, hypotension, etc

Front 438

pheochromocytomas

Back 438

-rare, most common type of neoplasm of adrenal medulla
-arise from chromaffin cells of paraganglion system
-secrete catecholamines to some degree
-rule of 10's:
-10% are outside the adrenal as paraganglions
-10% are bilateral in the adrenal
-10% are malignant
-10% arise in children
-10% occur in assoc with other endocrine neoplasms (like multiple endocrine neoplasia MEN) syndromes)
-most important sign is HTN

Front 439

neuroblastomas

Back 439

malignant tumors of primitive neuroendocrine cells related to chromaffin cells
-arise in adrenal medulla
-occur almost exclusively in young children, account for 15% of cancer deaths among children.
-some agressively malignant, others aren't.