GI, GU, Heme

Question 1

Explain the contents of blood?

Answer 1

Volume: 4-6L
RBC, WBC, platelets: 45%
Plasma: 55%. Water, proteins, enzymes, antibodies, clotting factors.
pH: 7.35-7.45

Question 2

Transports O2 on Hgb. Formation depends on?

Answer 2

Red blood cells, or erythrocytes.

Stem cells, bone marrow, iron, B12, folic acid, protein, B6, copper. Reticulocytes.

Question 3

Explain the making of RBC’s?

Answer 3

Kidneys detect reduced O2 carrying capacity of the blood. They respond by secreting erythropoietin (EPO) into the bloodstream. EPO stimulates erythropoiesis by the bone marrow. Addition of circulating erythrocytes increase O2 carrying capacity of the blood. Relives the initial stimulus that triggered the EPO secretion.

Question 4

Examples of white blood cells?

Answer 4

Monocytes, eosinophills, basophils, lymphocytes, neutrophils

Question 5

What diagnostic assessments are done for the blood?

Answer 5

Tests of cell number and function. CBC. peripheral blood smear. Coagulation studies: PT, INR, aPTT, anti-Xa assay. Coombs’ test. Serum ferritin, transferrin, total iron binding capacity (TIBC). Radiographic exams, bone marrow biopsy.

Question 6

Can be caused by a glucose-6-phosphate dehydrogenase deficiency anemia (G6PD). Or inherited.

Answer 6

Hemolytic anemia. Fever. Drugs/chemicals.
S/s include pallor and jaundice.
Treatment is to stop the offending agent, hydration, transfusion in severe cases

Question 7

This happens when the body attacks its own RBCs. May occur with other autoimmune disorders (SLE). Exposure of erythrocytes to antibodies.

Answer 7

Immunohemolytic anema, autoimmune hemolytic anemia.
Treatment depends on the severity of the s/s. Steroids. Immunosuppresasnts like cytoxan (more toxic) or imuran (less effective). Splenectomy to remove the site of destruction. Plasma exchange therapy. Transfusion for severe cases but may have issues with cross-matching.

Question 8

Most common type of anemia. Definite diagnosis by bone marrow aspiration. Diet, iron, preventative education. Etiology? Manifestations?

Answer 8

Iron deficiency anemia.
Bleeding (GI, menstruation). Malabsorption, inadequate iron intake/absorption, chronic alcoholism, partial gastrectomy, pregnancy, adolescent, infection, chronic bleeding.
May manifest as brittle nails, cheilosis, pica, smooth sore tongue.

Question 9

Manifestations of B12 deficiency?

Answer 9

Pallor, slight jaundice. Sore, beefy red tongue. Diarrhea. Neurologic s/s. Parestheis, proprioception, balance difficulty, cognitive dysfunction.

Question 10

What are common causes of folic acid deficiency anemia?

Answer 10

Malabsorption: celiac spure, chemotherapy.
Increased need: pregnancy, rapid growth.
Chronic malnourishment: elderly, alcoholics.

Question 11

Manifestations and treatment of folic acid deficiency anemia?

Answer 11

Pallor, SOB, fatigue, red smooth beefy tongue, cheilosis, diarrhea, no neurologic symptoms.
Treatment is supplementation and increasing the intake of green leafy veggies, fruits, meats, cereals

Question 12

The pathology of aplastic anemia? Diagnosis?

Answer 12

Bone marrow fails to produce blood cells, pancytopenia. Decreased RBCs, WBCs, platelets. Stem cells are injured.
Diagnosis includes CBC, bone marrow biopsy (very few cells, often replaced with fat)

Question 13

Treatment of aplastic anemia?

Answer 13

Blood transfusions, avoiding the offending agent, immunosuppressive therapy, splenectomy, stem cell transplant

Question 14

An increase in the number of RBCs above normal.

Answer 14

Polycythemia. Blood is hyperviscous.

Hematocrit is increased, 55% in males and 50% in females. Usually not secondary to dehydration.

Question 15

Excessive production of erythropoietin. Increases in RBCs, WBCs, platelets.

Answer 15

Polycythemia vera (PV).
Treatment is to give a repeat phlebotomy (2-5 times per week). Increased hydration. Prevent clot formation.

Question 16

Manifestations of polycythemia vera?

Answer 16

Skin and mucus membranes have a plethoric appearance (purplish or cyanotic). Intense itching, superficial veins visibly distended, HTN, increased risk for blood clots.

Question 17

A type of cancer with uncontrolled production of immature WBCs (usually blast cells) in bone marrow. May be acute or chronic. Cause is unknown.

Answer 17

Leukemia.
Lymphoid: stem cells that produce lymphocytes.
Myeloid: stem cells that produce nonlymphoid blood cells.

Question 18

Examples of types of anemia?

Answer 18

Acute Myelogenous Leukemia (AML)
Acute Lymphocytic Leukemia (ALL)
Chronic Myelogenous Leukemia (CML)
Chronic Lymphocytic Leukemia (CLL)

Question 19

Possible causes of leukemia?

Answer 19

Ionizing radiation, chemicals, drugs, bone marrow hypoplasia, genetic factors, immunologic factors (HIV, hep C)

Question 20

Treatment of leukemia?

Answer 20

3 phases of chemotherapy?
Induction: achieve rapid, complete remission of the disease
Consolidation: intent is to cure
Maintenance: maintain remiison. Not all types of leukemia respond to maintenance therapy

Question 21

What are the five phases of hematopoietic stem cell transplantation?

Answer 21

Bone marrow transplantation

Harvesting, conditioning regimen, transplantation, engraftment, post-transplantation recovery

Question 22

Bone marrow transplant (BMT) complications?

Answer 22

Infection, bleeding, failure to engraft.
Graft-vs-host disease (GVHD)
Veno-occlusive disease (VOD)

Question 23

Home management of care after a BMT?

Answer 23

Reduce risks of infection and bleeding. Reduce fatigue. Nutritional therapy, blood transfusions, drug therapy, energy management

Question 24

Cancer of the lymphoid tissue.

Explain Hodgkins and non-Hodgkins?

Answer 24

Lymphoma. Abnormal overgrowth of the lymphocyte after release from bone marrow. Solid tumors.
Both Hodgkin’s and non-Hodgkin’s cause similar s/s but they’re different. Main difference is the specific lymphocyte involved.
Reed-Sternberg cell makes it Hodgkin’s lymphoma. If it’s not present then it’s non-Hodgkins

Question 25

Clinical manifestations of Hodgkin’s and non-Hodgkin’s lymphoma?

Answer 25

Painless swelling of involved lymph nodes. s/s dependent on the location and extent of the cancer.
Hodgkin’s are more likely to begin in lymph nodes in the upper body (cervical, supraclavicular, medicinal nodes) but both types can be found anywhere in the body.
Weight loss, fevers, night sweats.

Question 26

Usually starts in single lymph node or in single chain of nodes. Spreads in an orderly manner. Very curable in early stages, high cure rate.

Answer 26

Hodgkin’s lymphoma (HL).
Most common in teens, young adults, and greater than 55 years of age.
Possible causes are viral and chemical agents.

Question 27

All lymphomas without Reed-Sternberg cells. Median age at diagnosis is 65 years. Start in the lymph nodes but can start in other tissues. Spreads in an unorderly manner to any organ.

Answer 27

Non-hodgkin’s lymphoma.
Swollen, painless nodes are the most common presentation, can be found anywhere in the body.
Diagnosis is a biopsy.

Question 28

Antibodies attack the body’s own platelets, enhances platelet destruction. Total number of circulating platelets is greatly decreased. Manifestations?

Answer 28

Autoimmune thrombocytopeniac purpura (ATP). Also known as idiopathic thrombocytopenia (ITP).
Production of platelets in the bone marrow is normal. Manifestations include large ecchymosis, petechial rash, bleeding, anemia.

Question 29

Diagnosis of autoimmune thrombocytopeniac purpura (ATP)? Treatment?

Answer 29

Low platelet count, anti platelet antibodies, megakaryocytes in the bone marrow.
Drug therapy: steroids, imruan, immunoglobulin IV, Platelet transfusion, splenectomy, safety.

Question 30

Autoimmune disorder with abnormal platelet aggregation in capillary beds. Decreased number of circulating platelets. Manifestations and treatment?

Answer 30

Thrombotic thrombocytopenia purpura (TTP).
Renal failure, MI, stroke, fatal without treatment.
Treatment includes plasmapheresis, immunosuppression with steroids, antiplatelet meds, fresh frozen plasma

Question 31

Unexplained decrease in platelet count after heparin treatment. Immune mediated clotting disorder. Previous exposure to heparin increases the chances of developing

Answer 31

Heparin induced thrombocytopenia (HIT).
Incidence is increased with heparin longer than 1 week, use of unfractionated heparin, post DVT prophylaxis, being female.

Question 32

Pathology of HIT?

Answer 32

Abnormal antibodies are formed, platelets are activated which form clots (called white clots). Platelets are destroyed leading to a decrease in the platelets.

Question 33

Manifestations of HIT? Diagnosis?

Answer 33

A thrombotic state develops with an increase in thrombin formation. DVT, PE, MI, CVA. Occlusion of limb arteries. End organ damage. Skin necrosis.
Platelet count is decreased during or after heparin therapy (less than 150,000 or less than 50% of the baseline). Functional assays detect platelet activation. Antigenic assays detect antibodies binding to the heparin complex.

Question 34

Management of HIT?

Answer 34

Stop the heparin!
Start alternative coagulation therapy: argatroban, angiomax, refludan. IV administration.
Monitor labs, observing for signs of thrombus formation in any organ system (renal dysfunction is common)

Question 35

Used for the treatment of anemia. Can have chronic renal failure. Stimulates erythropoiesis in bone marrow.

Answer 35

Epoetin alfa: Procrit, Epogen

Chemotherapy, decreased need for transfusions

Question 36

Explain epoetin alfa?

Answer 36

Side: headaches, body aches, diarrhea, irrational at injection site.
Adverse: chest pain, dyspnea, HTN, rapid weight gain, peripheral edema, MI
Implications: monitor frequent hbg, dosing based on it. Monitor vitals and for signs of improving anemia. Notify MD if BP is higher or hgb has reached normal levels.

Question 37

The most common oral cancer that is usually found on the lips. Can also be on the tongue, buccal mucosa, oropharynx. lesions are red, raised, eroded. Risk factors?

Answer 37

Squamous cell carcinoma.

Age, tobacco, alcohol, textile workers, plumbers, coal/metal workers, sun, poor oral hygiene, poor diet, HPV

Question 38

Cancer that’s usually found on the lips. Asymptomaitc. Starts with a small, scabbed area that doesn’t’ heal and advances to an ulcerated area with a pearly border.

Answer 38

Basal cell carcinoma.
High risk factor is the sun. Prevention includes dental screenings, decrease sun exposure, sun protection, eliminate tobacco, decrease alcohol

Question 39

Clinical manifestations of oral cancer

Answer 39

Unusual lumps or thickened areas. Red or white patches, sores that don’t heal. Soreness, pain, burning sensation. Trouble swallowing or chewing. Pain may radiate to the ear. Enlarged lymph nodes.

Question 40

Interventions for oral cancer?

Answer 40

Airway is the priority. Prevent aspiration, suction to clear secretions. Possible tracheostomy, oral care, nutrition.
Meds: steroids, antibiotics, humidified oxygen

Question 41

Treatment for oral cancer?

Answer 41

Radiation therapy, whose goal is to eradicate tumor while preserving function and appearance. May be given alone or with chemo and/or surgery.
Chemo, which may be given alone or with radiation or surgery. May receive more than one chemo agent.

Question 42

Causes of esophageal cancer?

Answer 42

Tobacco use, alcohol, long term and untreated GERD, high levels of nitrosamine and nitrates in food. Diets lacking in fruits/veg. Possible genetic influences with p53 gene. Biophosphonates.

Question 43

Clinical manifestations of esophageal cancer?

Diagnosis?

Answer 43

Dysphagia, pain, weight loss, painful swallowing, regurgitation, vomiting, foul breath, chronic hiccups, chronic cough, increased secretions, hoarseness.
Diagnosed with EGD with biopsy, CT scan, PET scan.

Question 44

Non-surgical interventions for esophageal cancer? Side effects of radiation therapy?

Answer 44

Dietary consult, daily weights, positioning, soft diet, thicken liquids, supplements, feeding tubes, protect from aspiration.
Acute esophagitis, odynophagia (difficulty swallowing), anorexia, n/v,.

Question 45

Pathophysiology of gastric cancer?

Answer 45

Most gastric cancers are adenocarcinoma. Liver, pancreas, esophagus, and duodenum are usually impacted. Metastasis through lymph to peritoneal cavity usually comes later.

Question 46

Causes of gastric cancer?

Answer 46

H. pylori, family hx, hx of gastric surgery. Increased risk with pernicious anemia, gastric polyps, chronic gastritis, slats, nitrates, smoking, alcohol.

Question 47

Prevention of gastric cancer?

Answer 47

Eradticate h. pylori. Heal gastritis, no smoking, limit alcohol, diet, genetic counseling with family history

Question 48

Diagnosis of gastric cancer?

Answer 48

History. Decreased h/h. Stool is positive for occult blood. Increased CEA. Upper GI series, CT scan, EGD, biopsy.

Question 49

Clinical manifestations of gastric cancer?

Answer 49

Asymptomatic possibly. Indigestion/ab discomfort. Epigastric/back pain. Weight loss. n/v, weakness, fatigue, anemia. Hepatomegaly, enlarged lymph nodes.

Question 50

Clinical manifestations of colorectal cancer?

Answer 50

Changes in bowel habits and stool. Anemia, rectal bleeding, gas pains, cramping, constipation, straining to have a BM, narrowing of the stool. Ab mass, hypoactive or absent bowel sounds, bowel obstruction

Question 51

Malignant tumors of the urothelium, most commony seen in the urinary bladder. Can affect the kidneys, renal pelvis, ureters, urinary bladder, and urethra. Most common in those greater than 60 years old.

Answer 51

Urothelial (bladder) cancer. Usually low grade. Multifocal. Recurrence up to 10 years.
Pts rarely seek treatment early, because early manifestations are painless. Hematuria often intermittent, found on routine urinalysis.

Question 52

Risk factors for urothelial cancer?

Treatment?

Answer 52

Smoking, exposure to toxins, well water, recurrent/chronic infections
Treatment is surgical excision then BCG virus installation to prevent reoccurrence. Possible intravesical chemo. Systemic chemo for metastases that can prolong life but rarely cures.

Question 53

Acute glomerulonephritis, aka?

Answer 53

Acute nephritic syndrome.. Usually preceded by infection. Most pts recover quickly and completely. Renal biopsy for precise diagnosis.

Question 54

Clinical manifestations of acute nephritic syndrome?

Answer 54

Hematuria, proteinuria, decreased GFR.
Mild to moderate HTN and edema. Fatigue, lack of energy. Azotemia: increased creatinine and BUN, anorexia, n/v.
In the elderly it’s often present with fluid overload.

Question 55

Interventions for acute nephritic syndrome or acute glomerulonephritis?

Answer 55

Treat s/s, preserve renal function. Manage infection with antibiotics. Monitor urine output, electrolytes, protein levels, fluid overload. Anti-hypertensives may be needed.

Question 56

This always leads to renal failure (CKD). Assessment is the same as with acute glomerulonephritis.

Answer 56

Chronic glomerulonephritis.

Slow progression. Eventually will need dialysis or transplant.

Question 57

Adenocarcinoma of the kidney. Clinical presentation varies greatly.

Answer 57

Renal cell carcinoma. Often asymptomatic or painless hematuria. Palpable mass, flank pain. Hematuria means a poor prognosis. Weight loss, anemia, increasing weakness.

Question 58

Surgical management of renal cell carcinoma?

Answer 58

Partial or radical nephrectomy. Renal artery embolization. Radiation, hormone therapy, chemo.

Question 59

Explain renal trauma?

Answer 59

80-90% blunt trauma to back, flank, or ab. Contusions, minor or major lacerations, vascular injuries. Often includes other organ injuries.

Question 60

Clinical manifestations of renal trauma?

Answer 60

Pain and renal colic, hematuria, mass/edema in the flank, ecchymoses, lacerations/wounds on the lateral ab or flank.
Renal hematoma is all of these plus tenderness of the lower ribs, upper lumbar vertebrae, flank, abdomen.

Question 61

Interventions for renal trauma?

Answer 61

Goals are to control hemorrhage, pain, and infection. Preserve/restore renal function.
Send all urine to the lab (RBCs), vital sings and h/h (shock), I/O (oliguria), frequent assessments