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Advanced Pathophysiology > TEST 1 > Flashcards

TEST 1 Flashcards

1
Q

Identify the WHO definition of health

A

State of complete physical, mental and social well-being and not merely the absence of disease or infirmity

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2
Q

Definition of Pathophysiology

A

The study of the abnormalities in physiologic functioning of living beings

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3
Q

Process of clinical reasoning

A

Steps in the thought process to get to your diagnosis

  • *Take a good history
  • *Develop DD list using +/- patient presentation
  • *Order diagnostics based on DD
  • *Prioritize the order of the differentials Possible vs Probable
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4
Q

Process of Differential Diagnosis

A
  • Most likely - prevalence demographics, risk factors, signs and symptoms
  • Life-threatening - can’t miss it
  • High prevalence - most common diagnosis
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5
Q

Etiology

A

WHAT CAUSED THE DISEASE

  • Idiopathic (unknown) Iatrogenic (treatment cause)
  • Risk factor (presence increased the likelihood of the disease)
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6
Q

Pathogenesis

A

Development or evolution of the disease from initial stimulus to full-blown disease and finish. Initial factors alter normal physiologic fx and lead to the development of clinical manifestations that are observed in a particular disorder/disease

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7
Q

Clinical course of a disease

A
  1. Exacerbation - a sudden increase in severity of existing disease
  2. Remission - decrease in s/s (could be cure)
  3. Convalescence - stage of recovery after a disease, injury, or surgery
  4. Sequela - complications resulting from illness (flu recovered but dev pneumonia)
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8
Q

Stages of disease

A
  1. Latent period - the time between exposure of pathogen and 1st s/s (asymptomatic)
  2. Prodromal period - 1st s/s occur indicating disease
  3. Acute phase -disease at full intensity; usually short-lived
  4. Exacerbation- sudden increase in severity
  5. Remission - decrease in severity, signs/symptoms
  6. Convalescence - stage of recovery after a disease, injury, or surgical procedure (rehab after stroke)
  7. Sequela - subsequent pathologic condition resulting from illness (pneumonia after flu)
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9
Q

Differentiate between primary, secondary, tertiary prevention

A
  • Primary - (P) Preventing disease: Seasonal flu shot, vaccinations, clean H2O, seatbelts, condoms, safe sex
  • Secondary (S) Screening, early detection: screening mammogram, blood tests, screening colonoscopy, year physicals
  • Tertiary (T) Medical Treatment (disease is there): medications, rehab, surgery, supportive care
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10
Q

Function of Organelles and its components

A

Control center containing all genetic information. Nucleus, Endoplasmic Reticulum, Golgi complex, Mitochondria, Lysosomes

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11
Q

Nucleus

A
  • Performs work maintaining the cell’s life
  • Largest organelle
  • Contains DNA and RNA synthesized in the nucleus
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12
Q

Endoplasmic Reticulum/Golgi Complex

A

Synthesize enzymes/proteins and packages them

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13
Q

Lysosomes

A

Digests material - Phagocytosis

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14
Q

Mitochondria

A

Converts energy for cellular reactions ATP production

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15
Q

Anaerobic vs. Aerobic metabolism in ATP production

A

Anaerobic no oxygen needed (not as efficient in ATP production) vs aerobic needs oxygen (more efficient)

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16
Q

Differentiate between diffusion, osmosis, passive/active transport

A
  • Diffusion - movement of solutes from higher to lower concentration
  • Osmosis - movement of solvent across cellular membrane from low to high solute area
  • Passive transport is diffusion and facilitated diffusion and moves fluid from higher concentration to lower concentration without ATP Active transport is movement from lower to higher solute concentration area it involves a carrier molecule (ATP- energy)
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17
Q

Describe active transport in relation to Na/K pump

A

Energy is required to move sodium out of the cell where the concentrations are high and move potassium into the cell where concentrations are high

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18
Q

Differentiate between function of DNA vs RNA

A
  • DNA replicates and stores genetic information. It is a blueprint for all genetic information in an organism.
  • RNA converts the genetic information stored within the DNA to a format used to build proteins and then moves it to the ribosomal protein factories
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19
Q

Identify the four types of cellular tissue

A
  1. Epithelial
  2. Connective
  3. Muscle
  4. Neural
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20
Q

Epithelial Tissue

A

Lines outside and interior areas of the body. Squamous, cuboidal, and columnar cell shapes. Holds together cushions organs

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21
Q

Connective Tissue

A

Large extracellular and fibroblast cells. Collagen, elastic, and reticular types Holds organs together, cushions organs

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22
Q

Muscle

A

​

  • Cannot replicate
  • Made of contractile fibers consisting of actin and myosin - Myocytes Smooth, cardiac, or skeletal
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23
Q

Neural Tissue

A

Cannot replicate

  • Neurons - conduct impulses
  • Neurons cell body, axon, dendrites
  • Neuroglial cells - supporting role
  • Astrocytes - BBB
  • Oligodendrocytes - myelin in CNS
  • Schwann cells - myelin in PNS
  • Microglia - phagocytic cells
  • Ependymal - produce CSF
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24
Q

Proliferation

A

The process by which cells divide and reproduce. The rate is determining factor. If the rate is abnormal develop neoplasms.

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25
Q

Differentiation

A

Process by which cells become specialized by:

  • Type
  • Function
  • Structure
  • Life cycle

Everything comes from stem cells

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26
Q

Adaptation

A

Cells attempt to prevent their own death from environmental changes through adaption. Modify size, numbers, and types in an attempt to maintain homeostasis. Adaption ceases once stimuli is remove. Atrophy - shrinks uses less resources Hypertrophy - enlarges Hyperplasia - increase # of cells (epithelial) - menses Metaplasia - adult cells are replaced by less mature cells. Cells still look alike. Initiated by chronic irritation and inflammation. Esophagus cells r/t GERD Dysplasia - mutation into cells of different size, shape, and appearance. Premalignant cell, next stage Ca. Can still be reversed

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27
Q

Describe the process of cellular injury and cellular death

A

Cellular injury is reversible up to a point. Cell death occurs by apoptosis or necrosis. Hypoxia is the most common cause of cellular injury. Apoptosis is programmed cell death at a certain point of development and there is no inflammatory response Necrosis - cell rupture, spilling of contents cause inflammation. Liquefaction (brain) cauceous (lung, TB), fat (pancreas), and coagulative (heart)

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28
Q

Explain the process of free radical damage and the role of antioxidants

A

Free radicals are unstable atom unipolar molecules in the body. The most concerning are those derived from oxygen and therefore called ROS. Free radicals attach to molecules and then make them unstable. Antioxidants are marketed as preventing and/or fighting disease and aging. Antioxidants travel through the blood vessels to reach damaged cells and supply the free radical with an electron to repair the free radical without damage to itself.

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29
Q

Differentiate between benign and malignant neoplasms

A

Neoplasm is cellular growth no longer responding to normal regulator processes (an error in the division of cells) Benign neoplasms are similar to normal cells faster growth than normal, localized, do not cause systemic effects. Malignant neoplasms are undifferentiated (nonspecific cell type), nonfunctioning cells that reproduce rapidly. Differ from normal cells in size, shape, and number. Invade nearby tissue and metastasize to distant tissue. Cause systemic effects. Genetic, epigenetic, and microenvironments factors. Epithelial - carcinoma Connective - sarcoma hematopoietic - leukemia Bone, liver, and lung most common areas of metastasizes

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30
Q

Identify common tumor cell markers

A
  • Alfa fetoprotein - liver, ovarian, testicular germ cell ca
  • CA 15-3 - breast, lung, ovarian, prostate
  • Carcinoembryonic antigen - bladder, breast, cervical, kidney, liver, lung, lymphoma, melanoma, ovarian, pancreatic, stomach, thyroid
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31
Q

Autosomal Dominant Disorder

A

Single gene mutation Passed from affected parent to offspring - REGARDLESS OF SEX

Ex. Marfan’s Syndrome - tall, thin, long arms, Aortic & Mitral valve murmurs, aorta abnormalities

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32
Q

Autosomal Recessive Disorder

A

Single gene mutation Passes from an affected parent - REGARDLESS OF SEX Both parents have to be carriers can skip generations before active disease occurs

Ex. Cystic Fibrosis

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33
Q

Sex-Linked Disorders Recessive or Dominant

A

Mostly X-linked Very little genetic material on Y chromosome. More males affected with more severe presentation

Ex. Hemophilia

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34
Q

Polyploidy

A

More than the normal 23 pairs in a cell

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35
Q

Aneuploidy

A

Abnormal separation during cell division - too many or too few chromosomes

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36
Q

Trisomy 21 Autosomal Aneuploidy

A

A spontaneous chromosomal mutation resulting in three copies of chromosome 21 Hypotonia Distinctive facial features Congenital heart defects Simian crease

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37
Q

Turner’s Syndrome

A

Females - deletion of X chromosome Short lymphedema of hands and feet Broad chest wide nipples Low-set ears

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38
Q

Klinefelter’s Syndrome

A

One or more extra X chromosomes and at least one Y (XXY) MALES

  • Small penis. prostate gland, and testes
  • Sparse facial and body hair
  • Long legs short obese trunk
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39
Q

Identify the components of the immune system

A

Antigen-Antibody Autoantibody

Primary Lymphoid Organs

Secondary Lymphoid Organs

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40
Q

Antigen

A

Foreign agents that trigger the body to produce antibodies

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41
Q

Antibody

A

Proteins in the body that IDs and neutralizes foreign agents (virus/bacteria)

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42
Q

Autoantibody

A

An antibody that attacks itself

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43
Q

Primary Lymphoid organs

A
  • Bone marrow - red marrow
  • Thymus gland
  • Lymphoid system Lymphocytes (T cells, B cells, Natural Killer cells)
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44
Q

Secondary Lymphoid organs

A
  • Spleen
  • Lymph nodes
  • Tonsils
  • Peyer patches
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45
Q

Describe the process of innate immunity

A

What we are born with. Interferons are released from cells that have an infected virus they put out this interferon to protect other cells from the virus. Bind to the plasma membrane to keep the virus from reproducing. Physical and chemical barriers found in the body Skin and mucous membranes (acidic skin and cilia) Natural Killer cells - react immediately Inflammatory response

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46
Q

Explain NK cells

A

Natural killer cells are not dependant on the thymus for development. Part of innate immunity will kill tumor and viral infected cells WITHOUT previous exposure. Do not need previous exposure to antigen. Will not affect cells with MCH1 protein to protect from autoimmunity

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47
Q

What role does the Thymus play in immunity?

A

Found in the mediastinum. Mature T lymphocytes that formed in the bone marrow.

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48
Q

Explain the sequence of the inflammatory response and the role of mast cells and mast cell mediators

A

Inital response is vasospasm to stop bleeding, clot, then vasodilates to get cells to help repair

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49
Q

Describe the complement system and the membrane attack complex

A

Plasma proteins to enhance and cause inflammation, gives chemotaxis (attracts neutrophils), lysis, and optimization (immediately flags cells for destruction shorter and faster than MAC) MAC creates a hole in a a bacterial cell membrane (mainly gram- bacteria)

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50
Q

Describe Adaptive Immunity and the difference between cellular immunity and humoral immunity

A

Recognized and destroy foreighn invaders and maintains a memory of it.

Cellular immunity (cell surfaces) T cells (CD4 and CD8) Humoral immunity (body fluids) B cells (memory or plasma cells) - mature in bone marrow and is aquired immunity. Floating around in the body looking for foreign invaders it remembers. Starts allergic rx’s, prevents viral infections, eliminates bacteria and toxins. ABLE TO RESPOND RAPIDLY found mainly in peripheral tissue. Thousands produced die rapidly. Requires activation from T Helper cells (CD4) No thymus prevents this step

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51
Q

CRP and Sed Rate

A

Labs to show inflammation in the body

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52
Q

Compliment cascade Classical Pathway

A

Triggered by the antibody-antigen complexes (IgG, IgM) starts at C1 ends with MAC but takes longer than the alternative pathway

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53
Q

Compliment cascade Alternative Pathway

A

Triggered by bacterial endotoxin. Skips classical pathway goes to C3 and involves opsonization (immediate flag for phagocytosis) its a shortcut

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54
Q

CD4 cells

A

Type of T cell, Regulator (helper) cell involved in Adaptive Immunity

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55
Q

CD8 cells

A

Type of T cell, Effector (cytotoxic) cell involved in Adaptive immunity

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56
Q

Major Histocompatibility Complex

A

Part of adaptive immunity that is Human Leukocyte Antigen (HLA) in humans Marks the body cells as “safe” No one person has the same MHC except identical twins MHC1 is on every cell expect RBC’s

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57
Q

IgM

A

Produced first! Lasts around 10 days M for immediate Active infection Activates complement system

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58
Q

IgG

A

Prior exposure to vaccine or virus. Can cross the placenta to provide immunity to the fetus (passive immunity)

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59
Q

IgA

A
  • Skin
  • MM
  • Saliva
  • Tears
  • Colostrum
  • Breast Milk
  • Acts locally
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60
Q

IgD

A

On B cells works with IgM

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61
Q

IgE

A

Triggers histamine and cell mediators Allergic reaction or parasitic infection

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62
Q

Passive Immunity

A

Immediate protection can be temporary Immunoglobulins (serotherapy) - Rabies, Hep A&B - gives immediate immunity Mother to the fetus (IgG, IgA)

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63
Q

Active Immunity

A

Has had infection or immunization

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64
Q

Explain the different types of vaccines

A

Live - identical immune response as infection - no for immunocompromised

Inactivated Vaccine - Whole/fraction of virus/bacteria/toxin, humoral immune response (Polio, HepA)

Fractional Vaccine - Modified toxins (Tetanus, Ptosis, Pneumonia)

Recombinant Vaccine - Genetically engineered (HPV)

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65
Q

Type I Hypersensitivity Reaction

A

Immediate response - Histamine, Leukotrienes, Prostaglandins Histamine (mild hives, eczema seasonal allergies to wheezing, tachycardia to anaphylaxis) IgE, Allergy response, Asthma, Anaphylaxis T Cells bind to mast cells, stimulate B cells

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66
Q

Type II Hypersensitivity Reaction

A

Transfusion reactions and newborn hemolytic reactions Destruction of antigens on target cells or tissues resulting in lysis B cells, RBCs, WBCs IgM and IgG are principal antibodies

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67
Q

Type III Hypersensitivity Reaction

A

Autoimmune disorders - accumulation of circulating antigen-antibody complexes - B cells Targets tissues, joints, skin, kidneys, blood vessels causing glomuleronephritis 10-12 days after infection and triggers complement system

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68
Q

Type IV Hypersensitivity Reaction

A

PPD reaction, Dermatitis

Delayed processing of the antigen by macrophages. Antigen presented to T cells after processing Can take 24-72 hours to develop

NOT ANTIBODY-MEDIATED

ex. Contact dermatitis, TB, poison oak

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69
Q

Immunodeficiency

A

Increases susceptibility to infections, crucial to prevent infections

  • Primary - congenital deficiency, defective CD4s, deficient complement system, deficient and defective adaptive system (sick more than you should be)
  • Secondary - loss of spleen, medications
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70
Q

Autoimmunity

A

Failure to identify self-antigens from foreign antigens Genetic component, exacerbation and remission, previous Epstein Barr infection. Two methods of attack: Autoantibody, T cell mechanism triggered by viral/bacterial infections, environ/occ stress

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71
Q

Opsonization

A

A pathogen is marked for ingestion and eliminated by a phagocyte, C3b and antibodies are responsible for opsonization

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72
Q

B Cell Disorders

A

B - Bone Marrow Attack invaders on the outside of the cell and antibody secretion Deficiency in humoral or antibody-mediated immune responses B cells recognize surface antigens of viruses and bacteria and produce and secrete antibodies, activating the immune system to destroy the pathogens. They defend against viruses and bacteria that enter the blood and lymph. IgA deficiency, hyper-IgM syndrome

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73
Q

T Cell Disorders

A

Deficiency in Cell-Mediated immune responses. Can only recognize viral antigens outside the infected cells T cells defend against pathogens including protists and fungi that enter the cells. DiGeorge Syndrome, Wiskott-Aldrich syndrome

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74
Q

Difference between CD4 and CD8 cells

A

CD8 (cytotoxic cells) can kill cancer cells recognizes antigens, destroys viral cells, mutant cells CD4 (T-helper cells) leads the fight against infection, , activates macrophages, interacts with antigens; stimulates B Cell proliferation and antibody production.

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75
Q

3 types of HOST / MICROBE RELATIONSHIP

A
  • Transient - food/water pass through without staying
  • Commensal - normal flora
  • Pathogen - cause disease
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76
Q

Physical barriers to pathogens

A

Epithelial cells (must be intact)

Sloughing of the skin

High-fat content of skin inhibits growth of bacteria & fungi

Mucous membranes trap

Cilia transport system in lungs sweep out

Frequent urine passes out bacteria

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77
Q

Biochemical barriers to pathogens

A
  • Acidic environment of the skin, urine, vagina inhibits bacterial growth
  • HCI in stomach kills organisms
  • Saliva, mucous, tears, sweat have enzymes that are antibacterial
  • Sebaceous gland secretions are antifungal
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78
Q

Risk factors that promote pathogen proliferation

A

Nutritional status, Age, Chronic Illness, Immunosuppression, Stress (cortisol)

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79
Q

Differentiate between high and low pathogen virulence

A
  • High virulence can cause disease in a healthy
  • individual Low virulence can cause disease in an immunocompromised individual
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80
Q

Routes of transmissions in pathogens

A
  • Direct
  • Indirect
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81
Q

Direct transmission (3) routes

A
  1. Body fluids: droplet
  2. Animal bites/soil
  3. Placenta transfer - vertical transmission
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82
Q

Indirect transmission (3) routes

A

​

  1. Vehicle borne - water, food, clothing, tissue
  2. Vector-borne - insect carries
  3. Airborne - droplets, measles, legionnaires (cooling towers)
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83
Q

Four types of pathogenic microorganisms

A
  1. Bacteria
  2. Viruses
  3. Fungi
  4. Parasites
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84
Q

Bacteria Characteristics

A

Various shapes Cocci (spherical) enterococcus

Bacilli (rod-shaped)

Vibrio (comma-shaped rods)

Pseudomonas Spirilla (twisted , spiral rod-shaped

Anaerobic - spirochetes

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85
Q

Viruses

A

Smallest known infective agents Composed of protein shell; capsid with core of DNA or RNA Some have protective envelope around the capsid Viruses have organelles bacteria don’t which means they can mutate into different strains

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86
Q

DNA Viruses

A

DNA - Produce messenger RNA in host cell nucleus Viral proteins formed from mRNA Virus DNA replicted by host polymerases Ex. HSV

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87
Q

RNA Viruses Retrovirus

A

Retrovirus: contains enzyme reverse transcriptase; convert their RNA into DNA; incorporated into the host’s DNA Ex HIV

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88
Q

RNA Viruses Replicating Virus

A

RNA viruses replicate within the cytoplasm and most produce mRNA which is then translated into proteins and genomic RNA, from which new viruses are created

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89
Q

Fungi

A

Have organelles Eukaryotic microorganisms with thick rigid cell walls Mycotic Infections caused by yeast Neutrophils, monocytes and eosinophils can destroy fungi Fungi thrive on glucose

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90
Q

Superficial (Fungi)

A

Superficial, dead, keratinized tissue, cause inflammation DO NOT INVADE TISSUE Ex. Tinea Pedis

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91
Q

Subcutaneous (Fungi)

A

Introduced during trauma Leads to ulcers and abscesses

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92
Q

Systemic (Fungi)

A

Inhalation of dust (from soil) More serious Affects immunocompromised hosts

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93
Q

Parasites

A

Establish themselves with another organism; benefit from the other organism Rarely transmitted by human contact Usually transmitted by a vector (malaria) Protozoal infections trans by food/water (Giardia) Commonly affect skin and GI tract

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94
Q

Protozoa

A

Single-celled parasite

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95
Q

Nemathelminthes

A

Roundworm parasite

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96
Q

Platyhelminths

A

Flatworm parasite

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97
Q

Five types of WBCs (Leukocytes)

A

_N_ever_L_et_M_onkeys_E_at_B_ananas

  1. Neutrophils
  2. Lymphocytes
  3. Monocytes
  4. Eosinophils
  5. Basophils
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98
Q

Neutrophils

A

First responders to infection or inflammation Count 2,500 - 7,500 Half-life 6-8 hours Bacterial Release toxins can damage normal tissues

99
Q

Lymphocytes

A

Immunity (B,T,NK cells)

Viral infections

Derived from Lymphoid stem cells Key cell involved in immune response

100
Q

Monocytes / Macrophages

A

Macrophages - Infection NON-GRANULOCYTES Monocytes are immature macrophages that circulate in the bloodstream and become macrophages in the tissue. Macrophages can ingest more than neutrophils and live from month to years. Capable of cell division

101
Q

Eosinophils

A

Allergic or Parasitic Infections 1/2 life 12 days Major fx is to kill intestinal worms (helminths) can’t be phagocytosed Release inflammatory enzymes and proteins

Half-life 12 days

102
Q

Basophils and Mast Cells

A

IgE Allergy In the bloodstream - Granulocytes (0-2% of WBCs) Basophil in connective tissue becomes MAST cell and can live months

BOTH cells contain histamine for allergic reactions have IgE receptors ASTHMA, ANAPHYLACTIC RX)

103
Q

Neutrophilia

A

High neutrophil count stored in bone marrow - infection - usually bacterial

104
Q

Bands or Granulocytes

A

Immature neutrophils that are in the bone marrow. They progress through the progranulocyte stage through myelocyte, metamyelocyte, band and mature neutrophil, each stage resulting in less RNA

105
Q

Neutropenia

A

Low neutrophil count often from chemo or radiation Iatrogenic neutropenia - caused by us (chemo/radiation)

106
Q

Macrophages

A

Mature monocytes Release cytokines to identify cells that dont belong (opsonization) Important in wound healing Important in antigen presentation Have C3b receptors to identify cells that have been opsonized

107
Q

Leukemia

A

Circulating tumors that involve the blood and bone marrow

108
Q

Lymphoma

A

Localized in the lymph tissue and disseminated to the other sites

109
Q

Plasma Cell Myeloma

A

Malignant transformation of B cell plasma cells; also forms localized tumors in the bony structures

110
Q

Left Shift of WBC

A

Immature bands are increased during infection. A left shift signals a big infection for days

111
Q

Neutrophil Storage Pool

A

Neutrophils are in bone marrow & circulating blood 10 days for neutrophils to mature Majority of neutrophils are in marrow Mature cells are sent out first

112
Q

Lymphoma

A

Localized in the lymph system and taken to other sites. Most common blood cancer

113
Q

Leukemia

A

Circulating tumors that involve the blood and bone marrow. Cancer of the leukocytes. Cells do not die as they should and create overcrowding for the healthy cells

114
Q

Plasma cell myeloma

A

Malignant transformation of B cell plasma cells; also forms bony tumors

115
Q

Plasma cell myeloma

A

Malignant transformation of B cell plasma cells; also forms localized tumors in the bony structures

116
Q

Hematologic Neoplasms

A

Based on cell type of the neoplasm instead of location. Used by WHO to classify Myeloid and Lymphoid Neoplasms

117
Q

Myeloid lineage neoplasm

A

RBC’s, platelets, monocytes, and granulocytes

118
Q

Lymphoid lineage neoplasm

A
  1. B cells
  2. T cells
  3. NK cells
119
Q

Pathogenesis of Hodgkin’s lymphoma

A

Typically starts in the lymph nodes of the upper body then spreads to other lymph nodes through lymphatic vessels. Node enlarges and compress surrounding tissue PAINLESS enlarged lymph node in neck and/or supraclavicular area; axilla, groin. Mediastinal mass/nodes on x-ray HAVE Reed-Sternberg Cells

120
Q

Pathogenesis of B/T cell lymphoma

A

90% of all lymphomas and 5% of childhood cancers DO NOT HAVE Reed-Sternberg Cells

121
Q

Hodgkin’s Lymphoma vs. B/T Cell and NK-Cell Lymphoma

A

90% of all lymphomas Older adults DO NOT HAVE REED-STERNBERG CELLS NH Lymphoma - painless enlarged lymph nodes in the neck or supraclavicular area; axilla, groin. Mediastinal mass/nodes on chest X-ray. Fever, night sweats, weight loss, splenomegaly

122
Q

Pathogenesis of Multiple Myeloma

A

Cancer of the plasma cells. Abnormal cancer cells migrate back to bone marrow increasing osteoclast (bone thinning) and abnormal “M protein” immunoglobulin. Bone pain is often in pelvis and pt has increased infections. Bone x-ray with show LYTIC lesions and they will have Bence Jones proteinuria

123
Q

Pathogenesis of MGUS (Monoclonal Gammopathy of undetermined significance)

A

Prior to Multiple Myeloma When normal plasma cells begin to respond abnormally to antigens. The abnormal plasma cells make monoclonal antibodies. Predisposes patients to develop MM

124
Q

Presentations of Acute Leukemia

A

Result of cytopenias (fatigue, SOB, bruising, bleeding, infections. Bone and joint pain Severe bone pain in children Lymphadenopathy, hepatosplenomegaly

125
Q

Presentations of Chronic Leukemia

A

Generally ASYMPTOMATIC presentation PAINLESS local or general lymphadenopathy Three phases for CML - Chronic, Accelerated, Blast Phase

126
Q

Identify the function and clinical process of Erythropoietin (EPO)

A

Regulator of red blood cell production. Produced in the bone marrow In response to hypoxemia and blood loss, supply the kidneys (liver in fetus) to produce EPO EPO is in the kidneys sends messages to the bone marrow

127
Q

Function of B12 & Folate

A

Necessary in the development of RBCs for cellular DNA synthesis. Deficiencies can lead to the inability of the cell to undergo nuclear division, premature apoptosis, and phagocytosis of precursor cells. Both from dietary sources.

128
Q

Explain RBC production

A

Produced in the bone marrow in response to erythropoietin Erythroblast (large nucleated cell) in marrow changes to reticulocyte in plasma with no nucleus (1% of RBCs) Reticulocyte matures in the bloodstream in 24-48 hours to become a mature erythrocyte RBC life span 80-120 days in plasma Biconcave disc shape with reverse deformability

129
Q

Discuss iron transformation process and the end role of ferritin

A

Dietary source absorbed in the duodenum and proximal jejunum. After absorption iron is bound, used, transported or stored. Transferrin binds and transports iron in the plasma and into the cell then Ferritin binds with Transferrin as stored iron in the liver as ferritin

130
Q

Transferrin

A

Transferrin is a protein that transports iron in the plasma. Transferrin iron receptor on the RBC cell membrane to pass iron into the cell.

131
Q

Hepcidin

A

Hepcidin controls how much iron is bound transported into the cells. Protein found in the liver. Regulated dietary iron uptake from GI. Allow or inhibits iron transport across cell membrane by binding to the transport. Low iron = less Hepcidin production. High iron = more Hepcidin production

132
Q

What is needed for DNA synthesis in the cells?

A

B12 and Folate

133
Q

What nutritional requirements are needed for erythropoiesis

A

B12, Folate, B6, Riboflavin, niacin, ascorbic acid, Vit E

134
Q

What is needed for B12 absorption?

A

Intrinsic factor secretion from parietal cells in the stomach

135
Q

Explain the role of reticulocytes

A

Reticulocytes are immature RBCs. Their number in circulation is an indicator of bone marrow response to anemia.

136
Q

What does a low reticulocyte count tell you?

A

May occur when the bone marrow is able to produce but cannot make RBCs such as iron, folic acid, vitamin B12, or erythropoietin. Reticulocyte count is an indicator of the status of RBC production

137
Q

What is Macrocytic RBCs

A

Larger than normal RBC. Macrocytosis is caused by nutritional deficiency, specifically of folate or vitamin B12. This can arise from a hereditary condition called pernicious anemia, in which a protein called intrinsic factor is lacking in your gut.

138
Q

What is Microcytic RBCs

A

Smaller than usual RBC. Causes of microcytosis are iron deficiency anemia and thalassemia

139
Q

What is hypochromic RBCs

A

Hypochromia means that the red blood cells have less color than normal. This usually occurs when there is not enough of the pigment that carries oxygen (hemoglobin) in the red blood cells. Can be caused by a lack of iron and B6 deficiency

140
Q

What is normocytic RBCs

A

Normal shape and size of RBCs but not adequate #s of circulating RBCs to carry O2 to organs. Usually the result of a chronic condition

141
Q

Define Anemia

A

Lack of RBCs. Impairs oxygen-carrying capacity of the blood, decreased RBC [production or increased RBC loss.

142
Q

Iron Lab Values

A

Normal 70-175 (m) 50-150 (f)

143
Q

TIBC Lab Values

A

Normal 250-450 mcg/dl If Fe is low TIBC is high If Fe is high TIBC is low

144
Q

Ferritin Lab Values

A

Normal 18-270 (m) 18-160 (f) Stores of iron - tells us how long the anemia has been going on. Chronic inf. conditions (autoimmune) Inflammation can raise ferritin levels falsely have to look at CRP and Sed Rate

145
Q

B12 Level Lab Values

A

Normal 280 - 1500 pg/mL

146
Q

Folate

Lab Values

A

Normal 3-13 ng/mL

147
Q

Retic count Lab Values

A

Normal 0.5 - 1.5% Immature RBC

148
Q

Iron Deficiency Anemia

A

HYPOCHROMIC - MICROCYTIC Increased TIBC, low MCV, low MCH, low MCHC, low iron, decreased ferritin. Inadequate iron supply for hemoglobin production. Iron intake or blood loss Problems with iron absorption

149
Q

Most common nutritional deficiency in the world. Women of childbearing age, Children <2yo, elderly

A

Iron Deficiency Anemia

150
Q

S/S Iron Deficiency Anemia

A

Cyanosis of sclera Brittle nails Koilonychia - spoon shaped nails Confusion - memory loss in elderly HA, pallor, fatigue, weakness, dyspnea, palpitations

151
Q

Vitamin B12-(Pernicious anemia)Folic Acid Deficiency (B9)

A

MACROCYTIC - NORMOCHROMIC Impaired DNA synthesis causes large developing cells. B12-lack of intrinsic factor Folate deficiency - dietary, alcoholism, cirrhosis High MCV, MCH, MCHC Normal Iron Low B12 Low Folate Low Retic count

152
Q

Vitamin B12-Folic Acid Deficiency S/S

A

Fatigue Glossitis (inflammation of the tongue) Peripheral neuropathy - paresthesia Dx. CBC, Serum B12 and Folate levels Iron studies (will be normal), Anti-intrinsic factor (to find out if you have antibodies to intrinsic factor shutting it down

153
Q

Anemia of Chronic Disease/Inflammation (2nd most common anemia)

A

NORMOCYTIC Caused by chronic diseases or inflammation Decreased RBC production by bone marrow Shortening of RBC survival Mechanisms underlying ACD Underlying disease as cause for clinical manifestations (Cancer)

154
Q

Anemia of Chronic Disease/Inflammation Diagnosis

A

Mild/Mod anemia (Low Hgb/Hct) Low iron, low reticulocyte count, elevated inflammatory markers (sed rate and CRP), low transferrin saturation

155
Q

Aplastic Anemia

A

Rare but serious Failure of bone marrow to produce cells - stem cell disorder. ALL LAB VALUES WILL BE LOW Leads to pancytopenia (leukopenia, erythrocytopenia, thrombocytopenia) Causes: Autoimmune (SLE, RA), chemo/radiation, viruses (EBV, CMV, HIV, Parvovirus), toxins, cancers Diagnosis: Bone marrow bx

156
Q

RBC destruction anemia Hemolytic anemia

A

RBC destruction in intravascular or extravascular space DIC, Transfusion Reactions, Thalassemia Hemolytic anemias - genetic - sickle cells, G6PD, autoimmune, infectious - malaria, idiopathic

157
Q

Thalassemia Anemia

A

MICROCYTIC Hereditary type of Hemolytic anemia. Abnormal hemoglobin for the abnormal quantity of one or two protein chains. Dx Positive family hx, low MCV, MCH, low Hgb/Hct, serum hemoglobin electrophoresis IRON LEVELS ARE NORMAL

158
Q

Beta Thalassemia

A

Mutation of HBB gene more common, categorized by severity of symptoms S/S: minor fatigue, pallor Mediterranean ethnicity, Middle East

159
Q

Alpha Thalassemia

A

Mutation in HBA1 and HBA2 genes, Not common S/S: Splenomegaly African American ethnicity

160
Q

G6PD Deficiency

A

A genetic disorder resulting in RBC membrane destruction Triggered by drugs (sulfa and quinolones) or infection. Affects males of African descent, X-linked recessive (males only) gene

161
Q

Etiology B12 deficiency

A

Inadequate intake - Vegan diet Inadequate absorption - Pernicious anemia (loss of intrinsic factor) Decreased utilization Use of certain drugs (metformin, antacids)

162
Q

S/S B12 deficiency

A

Neurologic deficits, slow insidious onset, smooth, sore tongue, normal folate, High HC MA

163
Q

Etiology Folic acid (B-9) deficiency

A

Alcoholism, overcooking food. Malabsorption, inadequate intake, parasitic infection, pregnancy

164
Q

S/S Folate deficiency

A

Same as B12 deficiency but NO NEUROLOGIC SYMPTOMS

165
Q

Identify the major causes of hemolytic anemias

A

Genetics - Sickle Cell, G6PD, Thalassemia, Autoimmune, Infectious (malaria), Idiopathic

166
Q

Pathology - Sickle Cell Disease and Dx

A
  • Abnormality in genes coding for globin portion of hemoglobin
  • Mutation of the HBB gene Inheritance of hemoglobin S from both parents
  • Dx hemoglobin electrophoresis
167
Q

Clinical manifestations of Sickle Cell disease

A

Significant anemia, pain, fatigue, irritability, pallor, jaundice from hemolysis Ischemia and necrosis (does not have reverse deformability, they get stuck)

168
Q

What factors can cause sickling in sickle cell patients

A

High intensity, exercise, high altitudes, dehydration

169
Q

What factors can precipitate hemolysis seen in G6PD?

A

Sulfa and quinolones (Cipro) or infection

170
Q

Define the pathogenesis of Polycythemia

A

An abnormal increase in erythrocytes and hemoglobin in the circulation can result in thick blood retarded flow and an increased risk of clot formation w/in the circulatory system

171
Q

Primary Polycythemia (Polycythemia vera) Etiology

A

Neoplastic bone marrow produces too many blood cells due to mutation in the JAK2 gene (Men, Caucasian, Older)

172
Q

Primary Polycythemia (Polycythemia vera)

Clin. Man

A

The absolute increase in RBC mass, leukocytosis, thrombocytosis, increased URIC ACID. Polycythemia vera is a panmyelosis because of elevations of all 3 peripheral blood components Hypertension & Splenomegaly Pruritus after contact with water Headache, erythematous palms, and soles GOUTY arthritis Vasomotor and microvascular thrombotic changes At risk for CVA, Stroke

173
Q

Relative Polycythemia (Polycythemia versa)

A

Increase in hemoglobin due to reduced plasma volume without an increase in red blood cell mass (dehydration)

174
Q

Secondary Polycythemia

A

Caused by factors other than an abnormal clone of erythroid progenitors. is the overproduction of red blood cells. It causes your blood to thicken, which increases the risk of a stroke. It’s a rare condition

175
Q

Triggers or causes of Secondary Polycythemia

A

Response to chronic hypoxemia, which triggers the increased production of erythropoietin by the kidneys. Obstructive sleep apnea, obesity hypoventilation syndrome, and chronic obstructive pulmonary disease (COPD).

176
Q

Pathophysiology of Clinical manifestations of Primary Polycythemia (Polycythemia Vera)

A

Theories include histamine release along with other cytokines or cool water contact causing vasoconstriction with prostaglandin and platelet aggregation

177
Q

Pathogenesis of iron overload (hemochromatosis)

A

Saturation of transferrin Iron binding to other proteins. Absorbed by cells that transform iron into reactive oxygen species in the liver, heart, pancreas, and joints. Chronic hepatitis causes increased ferritin and release of iron causing overload

178
Q

Hemostasis

A

HEMOSTASIS -The ability to stop small vessel bleeding after blood vessel injury Involves interaction with the vessel wall, circulating platelets (thrombocytes), and plasma coagulation proteins

179
Q

Fibrinolysis

A

FIBRINOLYSIS - lysis of fibrin to break down the clot. Factor XII and thrombin release plasminogen activators to form plasmin. Plasmin digests fibrinogen and fibrin and inactivates factors V and VIII. Protein S assists protein C in binding phospholipase and stimulates tissue plasminogen activation, initiating fibrinolysis

180
Q

The normal process for hemostasis

A
  1. Interaction between platelets and the endothelium of the injured vessel
  2. Vascular spasm
  3. Platelet aggregation to the endothelium
  4. Platelet plug formation (within 15 seconds)
  5. Clot formation
  6. Clot retraction
181
Q

Secondary hemostasis

A

Formation of fibrin clot through intrinsic and extrinsic pathways of coagulation. Final stage is clot retraction

182
Q

Clotting Factors

A
  1. Fibrinogen II
  2. Prothrombin III
  3. Tissue Factor IV
  4. Calcium V
  5. Proaccelerin VI
  6. Proconvertin VIII
  7. Antihemophilic factor IX
  8. Plasma thromboplastin X
  9. Stuart Prower XI
  10. Plasma thromboplastin antecedent XII
  11. Hageman factor XIII
  12. Fibrin stabilizing factor
183
Q

All clotting factor is made in the liver except

A

Factors 8 and 13 are not made in the liver

184
Q

What factors need Vitamin K

A

2, 7, 9, 10

185
Q

Where can you find Vit K in your diet?

A

Fat-soluble vitamin

Found in green leafy, cheese, butter

186
Q

What is needed in all but two steps of the cascade?

A

Factor IV Calcium

187
Q

What factor is associated with Hemophilia

A

Factor VIII

188
Q

What factor co-circulates with factor VIII to cause platelets to adhere?

A

Von Willebrand Factor

189
Q

How are the clotting factors numbered?

A

By order of discovery

190
Q

All factors are synthesized by the liver except

A

Factor VIII

191
Q

Differentiate between the intrinsic and extrinsic clotting pathway

A

The intrinsic pathway is initiated when blood comes into contact with altered vascular endothelium (inside the vessel) (PTT 33-45 sec - Play table tennis inside the house) Extrinsic pathway begins when the vascular wall is traumatized (PT 10-14 sec- Play tennis outside the house) Intrinsic and Extrinsic pathways lead to the common final pathway for clot formation

192
Q

PTT

A

Normal 33-45 seconds. Partial thromboplastin time used to evaluate the INTRINSIC, to common pathway XII to I. Used for managing Heparin infusion doses

193
Q

PT

A

Normal 10-14 seconds Prothrombin time is used to evaluate the EXTRINSIC pathway except for tissue factor (III)

194
Q

What Leukocytes are considered Granulocytes

A

Neutrophils Eosinophils Basophils

NeverEatBananas

195
Q

Immature Macrophage

A

Monocytes

196
Q

Immature Mast cell

A

Basophil

197
Q

Immature Neutrophils

A

Bands

198
Q

Basophils transfer into what once they are in connective tissue

A

Basophils in connective tissue are Mast cells and can identify allergins with IgE receptors quickly

199
Q

What WBC has C3b receptors for antigens that have been opsonized

A

Macrophages

200
Q

Patients with platelets < 20,000

A

Petechiae Bruising Bleeding gums Occult hematuria Retinal Hemorrhages

201
Q

Classical Hodgkins Lymphoma

A

Painless lymph nodes Reed Sternberg Cells Abnormal B lymphocytes Adults 20-4- years old Males > 55

85% - 5 yr survival rate

202
Q

3 types of B-Cell, T-Cell and NK-Cell Lymphoma

A

Aggressive: Diffuse lymphoma, Large B-cell, Burkitt Rapidly progress, Rapid mass growth Fever, Lymphadenopathy, night sweats, fatigue Indolent types: Follicular lymphoma, lymphadenopathy, hepatosplenomegaly Unorganized metastasis: everywhere

203
Q

Clinical manifestations of multiple myeloma

A

CRAB

  • Hypercalcemia
  • Renal Failure
  • Anemia
  • Bone lesions Bone pain Increased infections (suppressed B cells)
204
Q

When would you see Bence Jones Proteinuria and Lytic Lesions

A

Multiple Myeloma dx with Serum Protein Electrophoresis

205
Q

Two cell types of leukemia

A

Myeloid and Lymphoid

Myeloid - Adults

Lymphoid - Children

206
Q

How to diagnosis Chronic Leukemias

A

Routine blood count – Lymphocytosis, granulocytosis, monocytosis Peripheral smear Bone marrow biopsy - Blast stage >20% blast cells

207
Q

2 plasma proteins

A

Albumin and globulins

208
Q

What is the benefit of reverse deformability?

A

RBC can fit into tiny capillaries

209
Q

Transferrin

A

Carries and moves iron from the plasma into the cell

Uber for iron

210
Q

Where is RBC’s phagocytized?

A

Spleen

211
Q

Relative Anemia

A

Dilutional effect with normal cell numbers IV fluids, Pregnancy

212
Q

Absolute Anemia

A

Cell numbers are actually decreased

213
Q

How does the body compensate for anemia?

A

Tachycardia to increase cardiac output to vital organs. Increased erythropoietin activity in the kidneys

214
Q

Anemias resulting from destruction or dysfunction of RBCs

A
  • Thalassemia
  • Sickle Cell
  • G6PD
215
Q

MCV

A

Normal 80-94

Volume or size of RBC (Microcytic/Macrocytic)

216
Q

MCH

A

Normal 27-31

Color of RBC

(Normochromic/Hypochromi)

217
Q

What pts are at risk for polycythemia

A
  • COPD
  • Chronic lung disease
  • High Altitudes
218
Q

Intrinsic and Extrinsic clotting factors meet at what factor to work together

A

X - 10 then both use V, II, I

219
Q

Examples of endogenous anticoagulants

A
  1. Antithrombin III - inactivates thrombin
  2. Protein C & Protein S - both inactivates Factor V & Factor VIII
  3. Heparin = binds to ATIII
220
Q

Aspirin and Ibuprofen affect only:

A

Bleeding time

221
Q

D- Dimer

A

(<200 ng/ml) assess clot formation

222
Q

Thrombocytopenia Manifestations

A

Absent until platelets <100,000

  • Petechiae and purpura at <50,000
  • Deep tissue bleeding and intracranial bleed at <20,000
223
Q

The function of

Antithrombin III

A

Inactivates Thrombin

224
Q

What Factors are associate with the Triad of Virchow

A

Injury to the blood vessel endothelium

Abnormalities in blood flow

Hypercoagulability of blood

ALL lead to a state of increased coagulation this is seen in patients with PVD

225
Q

What clotting factor is associated with

HEMOPHILIA A (Classic)

A

Factor VIII

Factor 8

226
Q

Function of

Protein C & Protein S

A

Inactivates Factor 5 & 8

227
Q

Function of Heparin as an endogenous anticoagulant

A

Binds to AT III

228
Q

Peripheral Smear

A

Morphologic characteristics of platelet function

229
Q

How long do Aspirin and Ibuprofen affect platelet function?

A

Aspirin affects platelets for their life span

Platelets normalize 24 hours after the last dose of Ibuprofen

230
Q

Describe the different conditions associated with thrombocytopenia

A
  • Leukemia and other cancers
  • Some types of anemia
  • Viral infections, such as hepatitis C or HIV
  • Chemotherapy drugs and radiation therapy
  • Heavy alcohol consumption
231
Q

ITP

Immune Thrombocytopenic Purpura

A

Hypocoagulopathy state, when the immune system is destroying its own platelets

Secondary ITP causes: Autoimmune diseases, immunizations from live vaccine, infections, cancer

Autoantibody medicated development: IgG

Primary ITP: Most common cause

Acute: children 2-4 yo

Chronic: 20-50 yo women >men

232
Q

Common Manifestations

of ITP

A

Often asymptomatic

Abnormal bleeding - Petechiae/Purpura

Epistaxis, excessive bruising, Gi/rectal, menses

Diag made by exclusion

233
Q

TTP

Thrombotic Thrombocytopenic Purpura

A

In TTP damage to microvasculature and/or genetic predisposition can lead to plasma aggregation and thrombus formation. The platelet aggregation causes thrombocytopenia. The microvascular occlusion results in widespread ischemia to organs, presenting as fever, purpura, altered mental status, neurological signs, renal dysfx.

Often occurs as a result of deficiency in ADAMT513 enzyme

234
Q

Pathogenesis of

Von Willebrand Disease

A

Most common hereditary bleeding disorder

Deficient or absent VW factor

3 genetic types 1 acquired

Decreased VWF and Factor VIII (8)

  • Prolonged bleeding time & Prolonged PTT*
  • Normal platelet count & Normal PT/INR*
235
Q

Protein C Deficiency

A

Cerebral & ophthalmic thrombosis

Renal vein & umbilical thrombosis

Does not activate Factor V and VIII

236
Q

Protein S Deficiency

A

Autosomal dominant

Deep vein thrombosis and pulmonary emboli

Does not activate Factor V and VIII

237
Q

Factor V Leiden

A

Inherited

Genetic mutation that will not allow Factor V to be inactivated

Joint Intrinsic & Extrinsic pathway issue

238
Q

Converts Prothrombin to Thrombin & is the common pathway for Intrinsic and Extrinsic pathway

A

X

239
Q

Natural Active Immunity

A

Had the disease

240
Q

Artificial Active Immunity

A

Got Vaccinated

241
Q

Natural Passive Immunity

A

Mother gives to the infant in breast milk

242
Q

Artificial Passive Immunity

A

Giving you immune globulin or gamma globulin

243
Q
A
244
Q
A

Advanced Pathophysiology (8 decks)

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