patho final 2 Flashcards

Question

Acquired anemia- causes, s/s

Answer 1

[Acquired] drugs, toxins, venoms, immunohemolytic anemia, Rh- mom carrying Rh+ fetus -antibodies react w/antigens on RBC. -artificial heart valve, severe burns

Answer 2

Caused by low dietary intake, increased demand use of iron (pregnancy), slow or chronic blood loss (ulcer, period, cancer) impaired absorption S/S asymptomatic pallor skin + mucous membranes fatigue cold intolerance due to decreased cell metabolism palpitations, tachycardia, dyspnea delayed healing

Answer 3

large immature RBCS [Vitamin B12 deficiency anemia] [Folic acid deficiency anemia] Causes: -deficit in B12/ folic acids leads to impaired maturation of RBC -RBC released from bone marrow are large and nucleated, destroyed prematurely -Lack intrinsic factor - needed to absorb B12

Answer 4

caused by gastric atrophy -> decreased in parietal cells and the formation of intrinsic factor. Abnormal immune response resulting in destruction of gastric mucosa. inability to absorb B12 s/s typical manifestations of anemia; neurological signs -> tingling, burning sensation (paresthesia) in extremities -demyelination -loss of coordination

Answer 5

Causes malabsorption; celiac disease, antiepileptic meds dietary deficiency features similar to B12 deficiency but no neurological s/s

Answer 6

Bone marrow destruction -depression of bone marrow -> loss stem cells -decrease in RBC, WBC + platelets Causes onset insidious or severe radiation, chemicals, chemo, drugs that damage bone marrow S/S -those of anemia multiple infections excessive bleeding ecchymosis, petechiae

Answer 7

Involves both excessive clotting and excessive bleeding; massive release of erythropoietin and stimulates coagulation cascade. Massive damage and clots all over body. Causes: preeclampsia or eclampsia abruptio placentae (release of tissue thromboplastin from placenta) infection or shock carcinomas release substances that trigger coagulation major trauma blood transfusion reaction -> sepsis

Answer 8

Causes- inherited or acquired [Inherited] Hemophilia A: No factor xiii (8), Hemophilia B: No factor IX(9) Von Willebrand disease -> deficiency in Von Willebrand factor; most common hereditary [Acquired] -vitamin C + K deficiency, -Cushing's disease -senile purpura -warfarin -DIC S/S persistent bleeding, petechiae, purpura, ecchymosis, excess bleeding following minor tissue trauma

Answer 9

1) Vasospasm; vessel is damaged + constricts 2) Platelet plug formation: platelets sticky + stick to injury 3) Coagulation: clotting. Fibrinogen converts to fibrin. After wound heals, clot has to be dissolved.

Answer 10

Arteriosclerosis: Degeneration & narrowing of blood vessels as we age. Narrowing of small arteries and arterioles -> ischemia. Atherosclerosis: formation of atheromas/plaques in the vessel wall. The plaques have lipids, cells, fibrin & cellular debris; often have an attached thrombus. Initiating factor may be cell damage. If protective cap over plaque ruptures, clot/thrombus will form.

Answer 11

Obstruction of large arteries that supply your limbs. Due to atherosclerosis or inflammation leading to stenosis, thrombus, or embolism. S/S gradual onset pain while walking -> claudication (calf pain) foot cool to touch weak/absent pedal or femoral pulse when flow is severely reduced -> ischemia, ulcerations, gangrene

Answer 12

Crohn's: can affect any region of the GI tract from mouth to anus. Full thickness of bowel affecting the inner lining of mucosa, submucosa, and serosa. Leads to inability to digest + absorb foods chronic diarrhea go into remission, also have exacerbations, increasing risk of colon cancer. -Can scar intestine and result in intestinal blockage Ulcerative colitis: inflammation confined to the colon. only the mucosa lining may be affected develop edema, ulcerative sores bleed easily long term complication -> colon cancer

Answer 13

Abnormal drop in BP upon standing. Causes: 1) low blood volume - Baroreflex not efficiently working, dehydration 2) Autonomic dysfunction - ANS not working properly -drug induced, aging, bedrest, Most susceptible: elderly population, due to aging, autonomic function, dehydration

Answer 14

A spectrum of conditions that go from unstable angina to non-ST wave elevation MI to ST elevation MI. Anything causing reduced blood flow to heart and blocks it -> cardiac cells are dying. Characteristics: ECG changes - ST elevated, serum cardiac markers, proteins like myoglobin, creatinine kinase, and troponin released from necrotic heart cells

Answer 15

When there is a disruption in natural flora of LI. Seen in people on broad-spectrum antibiotics, where good bacteria in intestines are destroyed, allowing bad bacteria (C-DIFF) to overpopulate intestine. -acquired by oral-fecal route -acquisition of C. diff spores (when someone swallows them), the spores germinate(wakeup) leading to the overgrowth/toxin production -results in binding/damaging mucosa layer, causing hemorrhage + inflammation -antibiotic make LI susceptible of infection TREATMENT Stop current antibiotic treatment, treat w/antibiotic that will kill the C-Diff -metronidazole, vancomycin Fecal transplant/fecal bacteriotherapy

Answer 16

An abnormal immune response where the body reacts to non-harmful substances as though they are harmful and damage the body as a result. Type I: allergic reaction ‘allergic reactions’ -systemic or anaphylactic reactions -local or atopic reactions (genetic) urticaria (hives) rhinitis (hay fever) atopic dermatitis bronchial asthma -food allergies Type II: antibody mediated antibody mediated, the immune system targets and destroys cells/tissues by antibodies (IgG/IgE) binding to antigens on cell surface. Leads to cell destruction, inflammation, or dysfunction of the targeted cells or tissues. Type III: immune complex hypersensitivity Antigen antibody complex being deposited into the wall of the blood vessel, causing inflammation of vessel wall and damage. -free floating antigen + antibody [Systemic] autoimmune vasculitis, glomerulonephritis, serum sickness -urticaria(hives), patchy/generalized rash, extensive edema, fever Type IV: cell-mediated delayed hypersensitivity cell mediated- sensitized T-cells attack antigen. NO B CELLS Direct cell mediated cytotoxicity: Cytotoxic T cells directly attack and kill cells that contain an antigen. -viral infections (cytotoxic T) kill infected cells to eliminate the virus. Delayed-Type Hypersensitivity -takes a couple days for inflammation & adverse effects -IT helper cells & macrophages are involved in the inflammation and tissue damage. The body responds to soluble proteins from the antigen by recruiting these immune cells to the site of exposure. -TB TEST

Answer 17

When you have complete obstruction of a coronary vessel -> ST wave elevation MI Partial obstruction of a coronary vessel resulting in cardiac death -> non-ST elevation MI If troponin, cardiac marker appears, the person has had an MI. The higher the level of the enzyme/protein, the worse the cardiac damage. S/S - differ for men + women chest pain - radiating to left arm/neck sns - Gi distress (vomit, nausea), tachycardia, vasoconstriction, pallor, anxiety, restlessness, impending doom Hypotension, shock

Answer 18

When the heart cannot pump/fill w/enough blood to meet metabolic demands. It is usually secondary to another cause and is usually a chronic problem. Causes: 1)infarction, valve defect 2) HTN 3) lung disease 4)combination of factors S/S decreased CO, decreased blood supply to tissues fatigue, weakness, dyspnea, cold intolerance, dizzy BNP is a marker for heart failure, severity of heart failure, and whether or not treatments are working.

Answer 19

In hypertension or aortic valve stenosis, the heart thickens its muscle (hypertrophy) to pump more blood and overcome increased pressure. This helps maintain blood flow. However, over time, the heart becomes less efficient, needing more oxygen, which can lead to heart failure.

Answer 20

When the body cannot use glucose as energy source, so it uses fats and lipids. Incomplete metabolism of fats/lipids give rise to ketoacidosis. Cause- may start w/an infection or stress where the demand for insulin increases. Error in dosing (not giving self-enough insulin) or diabulimia s/s increased rate/depth breathing -sweet, fruity smell to breath -lethargy -decreased responsiveness -hyponatremia, hyperkalemia, low bicarb -severe hyperglycemia -low arterial pH -+ urine and serum ketones. Most susceptible

Answer 21

genetic condition where heart cells have a defect in contractile proteins and they do not have enough actin & myosin, heart cells work harder and hypertrophy. -cells too weak to function properly -To compensate for the weakness in individual cells, the heart muscle cells hypertrophy to do the same amount of work as normal cells. -The enlarged cells need more O2, but are less efficient at pumping blood, person is prone to heart failure and may suffer sudden death during exertion -MOST COMMON CAUSE OF CARDIAC DEATH IN ATHLETES -enlarged septum

Answer 22

Progressive cardiac dilation where the heart becomes enlarged 2-3x normal size. All 4 chambers of the heart are affected and the walls become thinned, impairing the hearts’ ability to pump blood efficiently. It’s easy for blood to enter but not leave

Answer 23

The heart muscle becomes stiff, preventing the heart from filling properly. -Restricted cardiac filling

Answer 24

A type of dilated cardiomyopathy that occurs in the last month of pregnancy or within 5 months of delivering. -half of women recover with no loss of cardiac function, half recover with loss of cardiac function -if mother gets it after 1 child, high risk of developing it with all children

Answer 25

[Acute Leukemia] -abrupt, rapid onset -high proportion of undifferentiated cells, immature, nonfunctional cells in bone marrow + circulation. More common in children. S/S fatigue, anemia, low grade fever, night sweats, weight loss, increased bleeding, bone pain, infection [Chronic] -high proportion of differentiated cells, mature cells -insidious onset, mild s/s, more common in adults. Rarely seen under 40. S/S slow onset, nonspecific symptoms, weight loss, weakness, leukocytosis, anemia, thrombocytopenia philadelphia chromosome i think idk. Most common in children: Acute mylogenous Most common in adults: Acute mylogenous chronic lymphocytic

Answer 26

Hodgkin's Lymphoma: defective B cells -> Reed Sternberg cells. Adults 20-40. Spreads from lymph node to lymph node and then organs. S/S: first indicator is large, painless, nontender lymph nodes: cervical. Later, splenomegaly + enlarged lymph nodes at other locations. Recurrent infections. Non-Hodgkin's Lymphoma: multiple lymph node involvement scattered throughout the body at diagnosis, metastasizes. More difficult to treat. Can be either B or T cells lymphoma. Multiple Myeloma: abnormal B cells. Idiopathic. Occurs in adults and involves plasma cells -proliferate/activate clasts -impaired blood cell formation, impaired antibody production s/s frequent infections bone pain multiple fractures anemia proteinuria, kidney failure

Answer 27

A DVT is a deep vein thrombosis. Blood clot that occurs in deeper veins, typically in the legs (femoral, popliteal, posterior tibial, and peroneal veins) -dangerous because clot can break off and lead to pulmonary embolism S/S Inflammation -pain -swelling -deep muscle tenderness -elevated wbc count -fever The first line of treatment is to dissolve the clot with tPA/ thrombolytic agent. After clot is dissolved you can put the patient on preventative measures like anticoagulants (blood thinners) and pneumatic compression devices.

Answer 28

Hypothyroidism thyroid gland doesn’t produce enough thyroid hormones. It can be congenital or acquired. -Hashimoto thyroiditis -thyroidectomy S/S Slow metabolism Weight gain w/loss of appetite Cold intolerant Bradycardia Muscle weakness Lethargy DECREASED T3/t4, TSH levels depend on where disorder originates, thyroid gland (primary) pituitary (2nd) Hyperthyroidism Hyperactivity of thyroid gland produces too much thyroid hormone. -‘thyrotoxicosis’ -caused by Grave’s disease & thyroid tumors -Type 2 hypersensitivity reaction -TSH- Secreting tumor of thyroid gland, increased T3/T4, enlarged thyroid gland -diffuse goiter, multinodular goiter S/S Hypermetabolism Weight loss Heat intolerant Tachycardia Exopthalmos T3/T4 increase TSH levels depend on where disorder originates, thyroid gland (primary) pituitary (2nd)

Answer 29

Intrinsic asthma/nonatopic is triggered by non-allergic factors, triggered by respiratory infection, cold, exercise, drugs (topic) Extrinsic: caused by allergens, trigger type 1 hypersensitivity reactions- IgE mediated S/S: -productive cough, marked dyspnea, tight feeling in chest, agitation, wheezing, thick mucus, rapid breathing, accessory muscle use, tachycardia Treatment 1) avoid trigger factors. Medications include inhalers (bronchodilators, such as albuterol) glucocorticoids/ leukotriene antagonists (to reduce inflammation) all above treat acute attacks Cromolyn sodium (a prophylactic medication that inhibits release of substances from sensitized mast cells and decreases hypersensitivity, but has no value during acute attacks, since mast cells already released histamine

Answer 30

Extreme case of hyperthyroidism. Seen in undiagnosed pt or pt who have not received adequate treatment. -Caused by physiological stress, infection, diabetic ketoacidosis, physical/emotional trauma, manipulation of hyperactive gland during thyroidectomy S/S very high fever (104-106) extreme tachycardia (>140) CHF, Angina, agitation delirium, confusion

Answer 31

Gigantism: excess GH before fusion of epiphyseal plates before puberty. -caused by pituitary-secreting tumor -If a pt has gigantism and issue isn’t resolved before they go through puberty, they will develop acromegaly & have both gigantism and acromegaly. -excess skeletal growth Acromegaly: GH excess after fusion of epiphyseal plates, after puberty. -pit-sec tumor + fusion ep. plates = acromegaly -exaggerated growth at ends of extremities

Answer 32

Primary TB: After inhaling TB bacteria, macrophages begin a cell-mediated immune response, leading to a Ghon focus containing macrophages and T cells. The bacteria are usually isolated in the Ghon foci and are inactive and not contagious. A positive TB test typically develops 3 to 6 weeks after the initial infection Latent TB: inactive/alive TB bacteria are contained within the Ghon foci. Individuals with latent TB test positive, not contagious. -if reactivates at subsequent date it becomes secondary TB Secondary TB: have latent TB, already have been exposed to TB. Reinfection from inhaled droplet nuclei. Reactivation of previously healed primary lesion. Now immunocompromised at later date and develop an active infection. positive TB test, contagious, pathogen in sputum -bacteria and IS damage tissues and create cavities. -signs of chronic pneumonia; gradual destruction of lung tissue -low grade fever, night sweats, anorexia, weight loss, sputum purulent, pathogen in sputum Miliary TB: This occurs from progressive primary TB leads to bacteria eroding blood vessels and spread through the body. Miliary TB lesions look like grains of millet in the tissues (found in muscle/milk) +TESTS: primary, latent, secondary contagious: 2ndary tb, miliary

Answer 33

-Seen in premature neonates born before type 2 alveolar cells are turned on. These cells produce surfactant. Premature infants born not producing enough surfactant will have difficulty inflating lungs. -lack of surfactant, infants can’t inflate their alveoli. -protein-rich fluid leaks back into alveoli and blocks oxygen uptake further.

Answer 34

metabolic acidosis, alkalosis, resp. acidosis, alkalosis

Answer 35

Nephritic syndrome is when the glomerular is affected and nephrotic is when basement membrane of glomerular cells are affected.

Answer 36

COPD: group of chronic respiratory disorders resulting in progressive tissue destruction and obstruction of the air passages. Can result in respiratory failure caused by severe hypoxia. May result in cor pulmonale (R sided heart failure due to lung disease) -chronic bronchitis -emphysema

Answer 37

Breakdown of alveoli wall, aveoli lose their elasticity because of an increase in elastase, due to migration of Eosinophils and Neutrophils in lungs. Normally what neutralizes elastase is alpha 1 tripson, but w/ increase in elastase, not enough inhibitor. Begins to break down alveolar wall. Fusion of different alveolar sacs. This loss of elasticity makes it easy to get air into lungs, but hard to get out. Loss of pulmonary capillaries. Loss of elastic fibers. Etiology/cause -Exposure to air pollutants -Smoking or genetic. Neutrophils in the alveoli secrete elastase. Increased neutrophils due to inhaling irritants, increase in elastase, damage alveoli by breaking down elastic tissue. Elastase decrease antitrypsin. Genetic: antitrypsin deficiency S/S Dyspnea Hyperventilation w/prolonged expiratory phase Anorexia Clubbed fingers w/secondary polycythemia Breathing w/pursed lips

Answer 38

Inflammation of the bronchi from cigarette smoke -obstruction of small airways -Changes in bronchi due to constant irritation from smoking/exposure to industrial pollution. -Effects are irreversible and progressive Characteristics: inflammation, obstruction, repeated infection, chronic coughing, increased number of mucus cells, hypersecretion of mucus, chronic, productive cough s/s constant productive cough shortness of breath mucus secretions thick and purulent cough more severe in morning bc mucus builds overnight airway obstruction, hypoxia, cyanosis

Answer 39

Air filled blister/bleb on the lung ruptures, air enters and separates pleura. (Atelectasis) Air moves into pleural space and ruptured bleb is sealed off. -primary - no disease -secondary - underlying disease present -No affect on unaffected lung with inspiration and expiration

Answer 40

hole or opening in the chest wall (often from trauma), and air enters pleural cavity through the wound on inhalation and leaves on exhalation. -The heart shifts towards the unaffected lung during inflation (mediastinal flutter), impairs venous return -Shifts back to affected lung during exhalation -decreases the amount of air entering the unaffected lung during inspiration (unaffected can’t inflate properly)

Answer 41

Most dangerous air enters pleural cavity through wound on inhalation, cannot leave on exhalation, so more and more air accumulates in the pleural cavity, compression of unaffected lung, mediastinum shifts to opposite side (unaffected lung), inferior vena cava gets compressed, venous return impaired significantly & CO reduced

Answer 42

yellowish discoloration of the skin because of high levels of bilirubin in the blood

Answer 43

diabetics, pt w/renal insufficiency, pt on nephrotoxic drugs, elderly, pt on NSAID, pt who had XRAY contrast

Answer 44

Creatinine is the best indicator of renal function. You have to lose 75% of kidney function before creatinine rises. BUN- blood urea nitrogen measure amount of nitrogen in blood if kidney fail, they can’t remove waste from blood

Answer 45

Allograft - transplant from same species to prevent rejection, IS drugs needed, match HLAs/MCHSs Isograft - transplant between identical twins no need for IS drugs no need to match HLAs/MHCs, since they are identical Autograft - transplant from one body part to another no IS drugs needed no need to match HLA/MCH Xenograft - transplant between different species IS drugs needed no matching for HLA/MHS

Answer 46

a type of tissue/organ rejection that occurs immediately as soon as blood flow has been established to the organ. Cause: host has preexisting antibodies in their blood that immediately attack the donor tissue/organ.

Answer 47

a type of tissue/organ rejection that occurs several weeks after transplantation when unmatched antigens cause a reaction cause: T cells recognize donor antigens as foreign and attack

Answer 48

a type of tissue/organ rejection that occurs months to years after transplantation. Blood vessels in the graft are gradually damaged.

Answer 49

ITP (Immune Thrombocytopenic Purpura) Cause: Immune system destroys platelets Main problem: Too few platelets → bleeding TTP (Thrombotic Thrombocytopenic Purpura) Cause: Platelets form small clots in vessels Main problem: Platelets used up → bleeding + clots

Answer 50

Platelets: Live 8–9 days in circulation Formed from megakaryocytes in bone marrow Stored in the spleen and released as needed Controlled by thrombopoietin (from liver, kidney, smooth muscle, bone marrow) How does deficiency cause bleeding disorder? Decreased platelet levels -> thrombocytopenia-> increased bleeding causes; Decreased production: Bone marrow failure (leukemia, aplastic anemia) Chemotherapy Infections Increased destruction: Immune thrombocytopenic purpura (ITP) – autoimmune antibodies destroy platelets Sequestration in the spleen Consumption: DIC or TTP (platelets used up in clots)

Answer 51

Cryocepitate is prepped from flesh, frozen plasma, concentrated clotting factors & is used when lack of clotting factors. Only give cryocepitate when patient is bleeding out and you do not know why. It is a treatment for bleeding disorders.

Answer 52

Cystitis is bladder inflammation and lower uti, Caused by bladder wall and urethra inflamed, red and swollen, may be ulcerated. Bladder capacity is reduced. Lower abdominal pain, Localized s/s -dysuria (pain/burn when pee) -frequency and urgency as inflamed bladder is irritated by urine Systemic s/s fever, general malaise, nausea, leukocytosis pyelonephritis is kidney inflammation and upper Uti 1or both of the kidneys involved. Infection involving the ureter, renal pelvis, and medullary tissue. -caused by E. coli, purulent exudate fills kidney pelvis and medullary tubules inflamed w/necrosis. -if severe, compresses the renal artery and vein and obstruct urine flow S/S -urinary casts consisting of leukocytes/renal epithelia. cells -dull, aching pain in the lower back, resulting from stretching of the renal capsule -chills w/mod-high fever

patho final 2 Flashcards

(76 cards)