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Hematology and Cardiovascular Disorders, Exams of Nursing

University of Pittsburgh (Pitt) - BradfordNursing

An overview of various hematological and cardiovascular disorders, including red blood cell aging, hemoglobin formation, anemia classification, sickle cell crisis, thrombocytopenia, and congenital heart defects. It covers the pathophysiology, signs and symptoms, and treatment approaches for these conditions. The document delves into the role of iron in hemoglobin formation, the effects of vitamin b12 deficiency, and the morphological classification of anemias. It also discusses the etiology of anemias, the impact of hemorrhage on the cardiovascular system, and the management of sickle cell crisis. Additionally, the document covers congenital heart defects, such as atrial septal defect, ventricular septal defect, tetralogy of fallot, coarctation of the aorta, and transposition of the great arteries. The information presented in this document could be valuable for students studying hematology, cardiovascular physiology, and related medical fields.

Typology: Exams

2024/2025

Available from 10/09/2024

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Pathophysiology Exam 3 Study Guide
Hematopoiesis ~9 Questions
Distinct features of erythrocytes, what they do, how they do it.
•
RBCs: responsible for oxygen transport.
o Once mature, have no organelles, no protein synthesis, do not go through mitosis.
Discoid in shape, flexible structure.
Life span changes, what happens as they age
•
Life span of 120 days, +- 20 days
o Altered by conditions, decreased in certain conditions.
o As RBCs age
▪
Lose flexibility
▪
Lysed or phagocytized
▪
Removed by the mononuclear phagocytic system.
▪
Erythropoiesis slows as we age.
Regulation of RBC
•
Requires hematopoietic growth factors (HGF)
o Growth factors
1. CSF- colony stimulating factors
a. cytokines that act as hormones
b. stimulate progenitor cells
c. stimulate maturation of cells
d. prevent apoptosis
2. EPO- erythropoietin
a. Hormone carried form kidney through blood to marrow.
b. released as response to hypoxia
c. stimulate uncommitted cells to become RBC’s
d. stimulate yellow marrow conversion to red marrow
3. IL-3++ (cytokine)
a. Regulate the reproduction, maturation, and functional activity of
blood cells.
b. increased with inflammation/infection
c. stimulate proliferation/maturation of immunocytes
4. Other cytokines/interleukins
5. Testosterone and Androgenic steroids-
a. hormones that stimulate leukocyte production.
b. Stimulate EPO, thereby increasing RBC’
c. Leads to increased erythropoiesis.
What is the significance of reticulocyte count (elevated, decreased, and/or normal) in the
context of anemia?
•
Reticulocyte count
o Indicates bone marrow response to anemia.
•
Increased
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Pathophysiology Exam 3 Study Guide

Hematopoiesis ~9 Questions

Distinct features of erythrocytes, what they do, how they do it.

  • RBCs: responsible for oxygen transport. o Once mature, have no organelles, no protein synthesis, do not go through mitosis. Discoid in shape, flexible structure. Life span changes, what happens as they age
  • Life span of 120 days, +- 20 days o Altered by conditions, decreased in certain conditions. o As RBCs age ▪ Lose flexibility ▪ Lysed or phagocytized ▪ Removed by the mononuclear phagocytic system. ▪ Erythropoiesis slows as we age. Regulation of RBC
  • Requires hematopoietic growth factors (HGF) o Growth factors
  1. CSF- colony stimulating factors a. cytokines that act as hormones b. stimulate progenitor cells c. stimulate maturation of cells d. prevent apoptosis
  2. EPO- erythropoietin a. Hormone carried form kidney through blood to marrow. b. released as response to hypoxia c. stimulate uncommitted cells to become RBC’s d. stimulate yellow marrow conversion to red marrow
  3. IL-3++ (cytokine) a. Regulate the reproduction, maturation, and functional activity of blood cells. b. increased with inflammation/infection c. stimulate proliferation/maturation of immunocytes
  4. Other cytokines/interleukins
  5. Testosterone and Androgenic steroids- a. hormones that stimulate leukocyte production. b. Stimulate EPO, thereby increasing RBC’ c. Leads to increased erythropoiesis. What is the significance of reticulocyte count (elevated, decreased, and/or normal) in the context of anemia?
  • Reticulocyte count o Indicates bone marrow response to anemia.
  • Increased

o New RBC’s produced and sent into circulation. (GOOD)

  • Decreased-problem o Compensatory mechanisms failed
  • Normal o Not normal in the anemic patient, should be increased in the anemic patient. Hemoglobin formation: heme, globins, oxygen carrying capacity.
  • Hemoglobin Synthesis o Hgb- the oxygen carrying protein of the RBC ▪ A single RBC contains as many as 250 billion hemoglobin molecules. o Globins- polypeptide chains ▪ Alpha chains (2) ▪ Beta chains (2) o Heme- Iron-protophoryn complexes ▪ 4 in Hgb ▪ Carry 4 O2 per each Hgb How is iron involved in hemoglobin formation? How is it brought into the body, stored, used? What are protophoryn and transferrin?
  • Iron o Required for RBC proliferation and Hgb synthesis o Absorbed form the duodenum and upper jejunum o Present within the plasma and extracellular fluid
  • Bound to transport protein, Transferrin o Helps get rid of 02 to cells. o Iron has to be properly charged, if not unusable.
  • Protoporphyrin o Organic compound that when complexed with ferrous iron, the molecule becomes heme.
  • Iron storage o Stored as ferritin ▪ Single iron chain o Hemosiderin ▪ See in bruising, gives blueish green color o Stored In ▪ Macrophages of the liver, spleen, bonemarrow. ▪ Hepatic parenchymal cells: tissue cells. What are the importance of Vitamin B12 and folic acid? Specific CNS symptoms of B deficiency.
  • B12 and Folic acid o Required to support proliferation and maturation of developing RBC o Deficiencies produce profound effects ▪ Cells are enlarged (macrocytic)

▪ EPO production o Cardiovascular ▪ With baseline vascular disease, sudden onset of localized ischemic manifestations. ▪ Elderly patients should be carefully monitored for angina, heart failure, claudication, severe GI dysfunction, or marked CNS symptoms even when Hgb is 10g/dL. o Hemorrhage ▪ Reduction in number in RBCs ▪ Fluids move form interstitial into vessels and plasma volume expands o Decreased viscosity cause more turbulent flow ▪ Ventricular dysfunction ▪ Cardiac dilation ▪ Heart valve insufficiency o Decreased oxygen delivery to tissues (skin) ▪ Delayed wound healing ▪ Loss of elasticity ▪ Early graying of the hair o Skin, mucous membranes, lips, nail beds, conjunctivae, palmar creases become pale.

  • Iron deficiency Anemia: how does it happen, how do different stages influence symptoms. o Most common type of anemia: worldwide o Developing countries more prevalent. o Blood loss of 2 - 4ml/day can cause anemia. o Occurs in Stages ▪ Stage I: body’s iron stores are depleted: few symptoms. ▪ Stage II: not enough Iron for BM, iron deficiency begins once iron stores depleted fully. ▪ Stage III: small deficient cells replace normal cells in periphery. - Progressive severe symptoms can progress to nerves and muscles.
  • Pernicious anemia: normochromic, macrocytic o Cause: malabsorption of B o Defective gastric secretion of intrinsic factor ▪ Congenital deficiency ▪ Adult onset atrophy of gastic mucosa ▪ Partial/complete gastrectomy. ▪ Has autoimmune component, attack cells of the gut, thus no intrinsic factor. o Mechanism ▪ Atrophy of guy - ETOH, hot tea, smoking ▪ Inflammation

▪ IF deficiency leads to inadequate B12 absorption (AUTOIMMUNE) o More than 90% of individuals demonstrate parietal cell autoantibodies.

  • Hemolytic Anemia: Normochromic-normocytic: know general concept of what happens o Erythropoiesis is normal, production is increased, but can’t keep up with destruction. o Acquired or Hereditary ▪ Genetics, trauma, toxins: snake venom, radiation, autoimmune reaction.
  • Sickle Cell- What causes sickling, how does it lead to ischemia, how to relieve a crisis o Point mutation changes amino acid in translation. ▪ Autosomal recessive o Thus protein can unfold and cause clumping o RBC sickles becomes brittle loses flexibility and clogs up vasculature. o Persistent hypoxemia causes further reduction in PO2 in the microcirculation, RBCs sickle o How to treat crisis ▪ Giving volume, warm body temp, allows cells to regain shape and resume normal function ▪ Limit crises to prevent long term organ damage.
  • Thrombocytopenia o Deficient number of circulation platelets o Most common cause of hemorrhagic disorders. o Congential or acquired: more common. o Results from ▪ Decrease or defective platelet production, or increased platelet destruction.
  • Idiopathic Thrombocytopenic Purpura (ITP) o Immunologic platelet destruction o Acute ▪ Post-viral thrombocytopenia ▪ Usually affects child ages 2 - 6 o Chronic ▪ Essential thrombocytopenia ▪ Adults older than 50, especially women 20 - 40. - Disseminated intravascular Coagulation (DIC) o Massive Endothelial damage: lots of procoagulation factors released. o Simultaneous clotting and hemorrhage: abprutio placenta. o Increased protease activity in the blood. ▪ Unregulated release of thrombin’ ▪ Subsequent fibrin formation and accelerated fibrinolysis o Activated thrombin > antithrombins. o Widespread Thromboses ▪ Organ hypoperfusion, ischemia, and infarction o Bleeding ▪ Depletion of clotting factors

a. Glands stimulate pituitary/hypothalamus to shut off the loop

  • Positive feedback a. Oxytocin – levels rise during birth Pituitary gland- hormones produced (anterior versus posterior), their actions. IV. Posterior Pituitary (Neurohypophysis) a. Hormones are synthesized in the hypothalamus and stored in the pituitary.
  1. Arginine vasopressin - water regulation (a.k.a. Antidiuretic hormone, ADH)
  2. Oxytocin - uterine contraction V. Anterior Pituitary (Adenohypophysis)
  3. Hormone secretion is under the control of releasing hormones from the hypothalamus.
  4. Hormones travel through the hypothalamic-pituitary portal system
  5. Hormones
  • Adreno corticotrophic hormone (ACTH)
  • Thyroid stimulating hormone (TSH)
  • Follicle Stimulating Hormone (FSH)
  • Luteinizing Hormone (LH)
  • Prolactin
  • Growth Hormone
  • Melanocyte Stimulating Hormone
  • Lipotropin
  • Endorphins SIADH- pathophysiology, and clinical presentation (particularly in relation to pathophysiologic mechanism) SIADH (Syndrome of Inappropriate Antidiuretic Hormone)
  • Etiology - Increased AVP (ADH)
  • **Body holds onto too much H20; Problems= fluid overload
  • Causes - Tumor tissue a. Head trauma b. Medications- morphine, nicotine c. Stroke
  • Clinical presentation d. Free water overload e. Decreased urine output f. Increased urine specific gravity g. Hyponatremia

DI- pathophysiology and clinical presentation (particularly in relation to pathophysiologic mechanism). nephrogenic versus neurogenic. Etiology - Decreased AVP (ADH)

  • Causes - Neurogenic (problem with synthesis/secretion) a. Tumor hypothalamus/pituitary b. Trauma c. Primary tumor d. Metastatic Cancer e. CNS infections- meningitis f. Medications
  • Causes - Nephrogenic (problem with receptor binding) a. Renal disease b. Renal transplant c. Heredity- receptors are fewer or less functional
  • Clinical presentation a. Dehydration b. Increased urine output c. Dilute urine d. Hypernatremia Physiologic axis- understand the HPA axis, primary versus secondary disease process. HYPOTHALAMUS PITUITARY THYROID ADRENAL GONADAL Hypothalamus produces neurohormones (ADH) that go down to pituitary
  • Hormones that kick things off Tertiary= Hypothalamus Dysfunction Secondary= Pituitary Dysfunction Primary= Gland Dysfunction (Thyroid, Adrenal, Gonadal) Thyroid hormones- T4, T3, and rT3. Also TRH and TSH. What they do, how they interact in normal and pathologic states. VI. Thyroid function
  1. Cellular metabolism
  2. Blood pressure maintenance

i. exopthalmia – bulging eyes j. enlarged gland/goiter IX. Hypothyroidism

  1. Inadequate circulating hormone
  2. Primary = disorder at the level of the thyroid gland (95%)
  3. Secondary/tertiary = disorder at the pituitary/hypothalamic level (5%)
  4. Causes a. Most common cause is surgical removal/ radioiodine ablation for the treatment of hyperthyroidism b. Idiopathic c. Hashimoto’s thyroiditis – inflammation causes hyperthyroidism and then scarring ultimately leads to hypothyroidism d. Hypophysectomy, pituitary radiation e. Stress states with pre-existing hypothyroidism (surgery)
  5. Clinical presentation a. bradycardia b. lethargy, decreased LOC, coma c. hypothermia d. hypoventilation e. decreased GI motility, constipation f. weight gain
  6. Myxedema coma a. extreme hypothyroid state b. interstitial accumulation of a mucopolysaccharide c. lowered metabolic rate X. Sick Euthyroid Syndrome
  • Not a thyroid problem
  • SES is adaptive response to non-thyroidal illness
  • T4 is converted to rT3 (physiologically inactive hormone)
  • Seen in 70% of hospitalized patients
  • No long-term bad effects; good thing HORMONE CONVERSION T

Energy RT3 T3 Normal Saving Path T Adrenal cortex- zones and associated hormones. Regulation of secretion of these hormones. Adrenal medulla- hormones; Adrenal insufficiency- Causes, patho and symptoms related to patho. IV. Adrenal Cortex

  1. Hormones a. Zona Glomerulosa – mineralocorticoids (aldosterone) b. Zona Fasciculata - glucocorticoids (cortisol) c. Zona Reticularus - androgens
  2. Regulation of secretions- HPA
  • Adrenal secretions manage:
  • Sugar
  • Energy
  • Fluid (RAA function/dysfunction) - aldosterone HYPOTHALAMUS - CRF PITUITARY - ACTH ADRENAL - (Glucocorticoids and androgens) V. Adrenal Medulla Hormones - Catecholamine’s
  • epinephrine (80%)
  • norepinephrine (20%) (precursor to epi) VI. Adrenal Insufficiency
  1. Sudden and severe decrease in levels of hormone
  2. Primary disease requires 90% loss of adrenal gland
  3. Secondary at the level of pituitary (lose ACTH)
  4. Causes a. Decompensation in patients with chronic adrenal insufficiency b. Destruction of the adrenal glands - hemorrhage (from HTN & TB)

b. tumorous adrenal cortical hyperfunction c. adenoma d. carcinoma

  1. Clinical presentations a. hyperglycemia b. redistribution of adipose tissue (moves from legs/arms to abdomen) c. decreased protein synthesis e. osteoporosis - weakened protein matrix f. impaired humoral antibody production – drop in immune function Edema- thin skinning; shiny skin Hyperaldosteronism- primary and secondary. Patho, cause and symptoms IV. Hyperaldosteronism
  2. Alteration in fluid and electrolyte balance
  3. Primary - excessive production in adrenal gland from either a tumor or hyperplasia
  4. Secondary - decrease in the pressure in the renal glomerulus activating the renin- angiotensin system
  5. Causes a. CHF b. cirrhosis c. nephrotic syndrome d. partial occlusion of renal artery
  6. Clinical presentations a. endocrine hypertension (2% of HTN – secondary) b. extracellular fluid expansion - Edema c. hypernatremia d. hypokalemia e. metabolic alkalosis – later stage; low K leads to Hydrogen exchange for Na Pheochromocytoma- major malfunction, causes, Symptoms related to patho. IV. Pheochromocytoma
  7. Tumor in the medulla (90%)
  8. Tumor of sympathetic ganglia
  9. Excessive production of catecholamines
  10. Clinical presentation a. hypertension - episodic b. headache – from HTN c. diaphoresis d. tachycardia e. weight loss f. emotionally labile

Diabetes Mellitus- Patho. Classifications. Cellular level patho. IV. DIABETES MELLITUS

  1. Overview a. Heterogeneous syndrome b. Glucose intolerance in common
  2. Classifications a. Type 1 - lack of endogenous insulin production i. loss of beta cells in islets of Langerhans ii. immune mediated or idiopathic iii. 10% of cases, juvenile to adult onset iv. LADA v. HLA genotypes vi. Environmental exposures (viral, diet) vii. Prone to ketoacidosis b. Type 2 - insulin resistance and receptor deficit i. receptor driven? ii. genetic factors iv. environmental factors- high sugar diet, high saturated fats/transfats, obesity, lack of exercise. ‘Urban lifestyle’ v. ‘Prediabetes’ - Founder’s Effect- same people mating allowing genes to propogate c. Secondary i. surgery ii. glucocorticoids iv. pancreatic disease d. Gestational i. Type 2 like ii. 2 - 10% of pregnancies iii. May resolve after pregnancy- 90 - 95%
  3. Insulin a. Anabolic hormone b. Major sites - liver, muscle, adipose tissue (red blood cells and brain cells do not require insulin) c. Cellular actions (KNOW THESE) i. Increases Glucose uptake ii. Increases Protein synthesis iii. Increases Carbohydrate Metabolism iv. Decreases Fat Metabolism
  1. Pathogenesis a. Hyperglycemia b. Intracellular and extracellular volume deficit
    • Will try to dump extra glucose by diuresing
    • Pulled first out of blood stream, then extracellular, then intracellular
  2. Clinical Presentation a. Polyuria and polydypsia b. Hyperglycemia (1200 mg/dl +) (over periods of weeks) c. Altered level of consciousness/coma d. Mortality rate 40 - 70% Severity of hyperglycemia is a factor Hypoglycemia- Patho and symptoms related to patho. IV. HYPOGLYCEMIA
  3. Overview a. Inadequate circulating glucose b. Defined as a blood glucose of < 50mg/dl
  4. Clinical Presentation a. Adrenergic i. anxiety – impending doom ii. sweating iii. hunger iv. tachycardia b. Neuroglycopenic i. confusion ii. weakness - generalized iii. slurred speech iv. seizures Somogyi phenomenon- Patho and symptoms related to patho. Somogyi phenomenon a. Rebound hyperglycemia Glucose drops steadily until 3 - 4am then spikes high b. Clinical presentation i. nightmares ii. morning headaches iii. inconsistent glucose levels/elevated am glucose Food right before bed might help

Cancer cell and Dysfunction (~ 11 Questions)

Phases/stages of carcinogenesis and factors associated with phases

  • Cancer is genetic disease that consists of different combinations of genetic alterations. It takes SEVERAL different types of alterations to contribute to malignant changes in the cell. Most cancers are sporadic and NOT hereditary. Stages of Carcinogenesis
    1. Initiation a. Carcinogen interacts with/damages DNA b. Repair can occur after this point and can be REVERSED c. Initiating event is genetic mutation oncogene
    2. Promotion a. Reproduction or proliferation of damaged cells, forming a mass of cells or benign tumor b. At beginning removal of promoting agent can stop the expansion of tumor mass c. Reversible in early stages
    3. Progression a. Irreversible b. Involves a number of sequential mutations in genes including oncogenes and tumor suppressor genes c. End result is tumor malignancy 6 Hallmarks of Cancer
  1. Evasion of Apoptosis – produce IGF survival factors
    • **One of most important factors for survival of cancer (live longer, grow faster)
    • **P53 Gene – commonly mutated tumor suppressing genes – responsible for evasion of apoptosis
  2. Self-Sufficiency in growth signals – activate H-RAS oncogene
    • Modulation of extracellular growth signals
    • Alteration of trans-cellular signal transducers (surface receptors)
    • Deregulation of intracellular signaling pathways (such as RAS)
  3. Insensitivity to growth inhibition signals – Lose Rb suppressor
    • Most/All anti-proliferative signals are funneled through retinoblastoma (Rb)
    • TGFB suppresses cell growth
    • Downregulation of Smad 4

N0: absent from regional lymph nodes N1-3: degree of spreading M- metastasis; describes distant metastasis M0: no distant metastasis M1: metastasis to distant organs G- degree of differentiation G1: well differentiated G2: moderately differentiated G3: poorly differentiated G4: undifferentiated Theories related to Cancer: Double Hit theory, Seed and Soil Hypothesis Seed & Soil Hypothesis

  • Tumor Cells (Seed); Distant Tissue (Soil)
  • Hypothesis that suggests certain cancers metastasize to certain tissues where they like to grow. For example, lung cancer will metastasize to brain, but not breasts. Breast cancers will metastasize to lung.
  • Grow where they are happy
  • TSG and Oncogenes do not play role in development of metastasis Double Hit Theory 1 st^ Event - Initiation
  • Carcinogen = Initiatior 2 nd^ Event – Promotion
  • Agent = Promoter
  • Lag period- time between exposure (first hit) and development of clinically apparent cancer Viruses and cancer- relationship 7 Different Viruses Related to Cancer
  • Epstein-Barr b cell lymphoma, nasopharyngeal cancer
  • Hepatitis B & C liver cancer, non hodgkins; from recurrent infections
  • Human Papillomavirus cervical, anal, oropharyngeal cancer
  • Human T-cell lymphotropic
  • Kaposi’s Sarcoma Herpesvirus
  • Merkel Cell Polyomavirus Bacteria: H. pyloria stomach cancer
  • Chronic Inflammation- can damage DNA, proteins, cell surfaces
  • Interaction with Cellular DNA- activates genes that promote growth of tumors or inactivates genes that prevent tumor growth
  • Immunosuppression- decreases efficiency in recognizing cancer cells

Discuss progression of cancer- angiogenesis

  • Every tumor has to learn/acquire angiogenesis or they will not survive*
  • Angiogenesis- induction of blood vessel growth
  • Anti-Angiogenesis:
    • Inhibit endothelial cells that line the blood vessels
      • Endostatin, Combretasatin A4, Thalidomide
    • Inhibit angiogenesis signaling cascade
      • Bevacizumab, Interferon Alpha
  • Block endothelial cells from breaking down extracellular matrix
  • Marimistat, Neovastat Latency period Can be up to 20 years or more
  • From initiation up until malignancy Tumor suppressor genes Act to stop cell growth – prevent cancer
    • **P53- transcription factor that regulates cell division/death
    • Rb- alters activity of transcription factors (controls division)
    • APC- controls availability of transcription factors Characteristics of tumor cells
  • Senescene- limits the total number of times cells can reproduce themselves
  • Identifiable at 1 gram in size and 30 population doublings; slows down by detection Gompertzian Equation- most tumors originate 2 years prior to detection
  • 30 doublings= clinically detectable; 7 th^ & 10 th^ doubling = metastatic potential C hange in bowel/bladder habits A sore that does not heal U nusual bleeding or discharge T hickening or lump in the breast, testicles, or any part of the body I ndigestion or difficulty swallowing O bvious change in a wart, mole, or skin condition N agging cough or hoarseness Cancer prevention- proto-oncogenes Proto-oncogenes- stimulate cell to grow, divide, and move through cell checkpoints
    • Mutation leads to oncogenes that do not go through checkpoints
    • Oncogenes= bad (HER-2, EGFR, RAS) Cancer treatment: targeted therapy, stem cells, all those discussed Local- surgery, radiation Systemic- chemo, targeted therapies, immunotherapy