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Pathophysiology > Module 4 & 5 > Flashcards

Module 4 & 5 Flashcards

1
Q

Aneurysm (Main points)

A
  • Arterial Bulging
  • Causes
    • Brain – Berry Aneurysm
    • Age, HTN, Smoking, Genetic – AV malformation
    • Abdominal Aorta Aneurysm (AAA) – HTN, smoking,
      Marfan’s Syndrome (connective tissue disorder), athelrsclerosis (plaque build up), FHx
  • Signs and Symptoms
    • Brain – HA, eye pain, visual changes, numbness/ weakness face, ALOC > Increased ICP
    • Abdominal Aorta > pain in abdomen and back, abd. mass, anxiety, N/V, diaphoresis, tachycardia, shock
  • Testing
    • CT/MRI
    • Cerebral arteriogram
    • Abd. US
      ALOC=altered level of consciousness
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2
Q

Peptic Ulcer

A
  • Ulcerations of stomach lining
    • Gastric - stomach
    • Duodenal – small intestine
    • Esophageal > GERD
  • Causes
    • H.pylori , NSAIDS (>50%), Smoking, Stress, EtOH
  • Signs and Symptoms
    • Gnawing or acute abd pain
    • N/V, Weight loss, Hemoptysis, Melena (black tarry feces)
  • Testing
    • Upper GI
    • Endoscopy
    • H.pylori > blood, breath, stool
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3
Q

Hematuria

A
  • Blood in the urine
  • Causes
    • UTI, pyelonephritis, nephrolitihiasis, Benign Prostate
      Hyperplasia (BPH), trauma, medications (aspirin, blood thinners, penicillin), malignancy, bleeding disorders, strenuous exercise
    • Post-streptococcal glomerulonephritis - common cause in children
    • False positives: discoloration (certain drugs, Ex-lax, beets, rhubarb, berries), contaminated urinary catch (menstrual bleeding)
  • Signs and Symptoms
    • Often painless
  • Testing
    • UA,
    • CT, MRI,
    • US,
    • Cystoscopy
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4
Q

Fibrinolysis & anticoagulants

A
  • Fibrinolysis = breaking a clot apart
    • Tissue Plasminogen Activator (tPA):
      • Activate Plasminogen
    • Plasminogen Produces Plasmin:
      • Digests Fibrin Strands
  • Anticoagulants = clot busters
    • Antithrombin III (From Liver) Deactivates Thrombin Before It Can Act On Fibrinogen
    • Heparin (From Basophils And Mast Cells) Activates Antithrombin III
    • Warfarin (Coumadin)
    • tPA activates plasmin to degrade clot
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5
Q

Bleeding test time

A

This test measures the time taken for blood vessel constriction and platelet plug formation to occur. No clot is allowed to form, so that the arrest of bleeding depends exclusively on blood vessel constriction and platelet action.

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6
Q

Hemophilia

A
  • Rare inherited (genetic) bleeding disorder in which your blood doesn’t clot normally
  • Almost always occurs in males –XY, no back up copy to make clotting factor
  • Certain clotting factors in the blood are either insufficient or missing
    • Type A: 80% - clotting factor VIII
    • Type B: 15% - clotting factor IX
  • Hemophiliacs bleed longer, NOT faster
  • Increased (A)PTT
  • Seen when born, umbilical cord bleeds excessively
  • Infant stage - more bruising with mild irritation
  • Older - Nose bleeds, easily bruised, blood in urine, severe joint pain brought upon by blood in the joint cavities
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7
Q

Von Willebrand’s Disease

A
  • Most common inherited bleeding disorder
  • Varied genetics - can be AUTOSOMAL DOMINANT - women can get it too
  • Incidence 1:100 to 1:1000
  • Easy bruising and mucocutaneous bleeding
  • Defective primary hemostasis
  • Decreased adherence to vascular injury
  • Inadequate platelet plug prolongs Bleeding Time test
  • Normal (A)PTT and PT tests
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8
Q

DIC (Disseminated Intravascular Coagulation)

A
  • State of hypercoagulation; thrombosis & hemorrhage occur simultaneously
    • Widespread clotting leading to ischemia and multiple end-organ failure.
    • Clotting consumes platelets & clotting factors leading to hemorrhage.
  • Causes: sepsis, bacterial infections, cancer (hematalogic and solid tumors), retained placenta or placental abruptions, anesthesia, burns, major trauma
  • Signs and Symptoms: bleeding, bruising, hypotension, thrombocytopenia
  • Testing: Prothrombin time (PT), Partial thromboplastin time (PTT), Platelet count, Fibrinogen, D-dimer, Fibrinogen/fibrin degradation products (FDP)
  • Poor prognosis; high mortality rate
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9
Q

DIC - Initiating Mechanism

A
  • Release of TF (tissue factor or tissue thromboplastin) into circulation
  • TF not normally in contact with blood
  • TF released in response to vascular injury, cytokines, bacterial endotoxins
  • TF binds with coagulation factors that trigger coagulation pathways
  • Excess thrombin cleaves fibrinogen which leaves behind fibrin clots
  • Clots trap platelets, form bigger clots, thrombosis, ischemia, end-organ damage
  • Decreased fibrinolytic activity & diminished plasmin activity
  • Clot factors & platelets consumed, fibrin degradation products (anticoagulants) create risk of hemorrhage
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10
Q

DUB - Dysfunctional Uterine Bleeding

A
  • Menorrhagia - prolonged, excessive bleeding at regular intervals
  • Metrorrhagia - irregular, frequent uterine bleeding
  • Menometrorrhagia – combo. of above
  • Polymenorrhea - regular bleeding
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11
Q

Leiomyoma

A
  • Uterine Fibroids (Benign smooth muscle tumors)
  • Causes
    • Genetic, Hormonal, Idiopathic?
  • Signs and Symptoms
    • Menorrhagia (abnormal heavy menstruation), Dysmenorrhea (painful menstruation), Metrorrhagia (abnormal bleeding from uterus)
    • Pain, pressure in lower abdomen, urinary frequency, constipation, backache, abdominal fullness, cramping with periods, Enlarged and asymetrical uterus on pelvic exam
  • Testing
    • Transvaginal US, CBC, hormone levels, endometrial biopsy (to rule out cancer)
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12
Q

Endometriosis

A
  • Abnormal growth of endometrial tissue outside uterus
    • Usually found on ovaries, fallopian tubes, outer uterine wall, intestines, abdominal organs, rarely beyond (pleural cavity)
    • Tissue responds to hormones - thickens, breaks down, bleeds, irritates
  • Causes
    • Unknown, Hormonal, Fetal Development, Family Hx, Caucasian, Asian
  • S/S
    • Onset after menses and stops after menopause
    • Pelvic pain, Infertility (adhesions may block), Dysmenorrhea, Menorrhagia, dyspareunia, GI S/S
  • Testing
    • Exam, US, Laparoscopy, R/O  other causes of DUB, pelvic pain
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13
Q

Endometriosis - Hypotheses

A

Most widely-accepted theory: transplant of endometrial cells from uterus to other sites via:
Backflow of blood containing endometrial cells (avoid yoga inversions during menstruation) transport to intra-abdominal sites
Circulatory & lymphatic transport to distant sites
Other theory: Cells in abdomen retain ability to differentiate into endometrial cells
Incidence increased with first degree relatives
Dysfunctional immune response
Potential protective factors: multiple pregnancies, use of low-dose oral contraceptives (continuous or cyclic), and regular exercise (especially if begun before age 15, if done for > 7 h/wk, or both).

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14
Q

An aneurysm is a?

A

Localized dilation or outpouching of a vessel wall or cardiac chamber

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15
Q

True aneurysms

A

Involve all three layers of the arterial wall & are best described as a weakening of the vessel wall. Most are fusiform and circumferential, whereas saccular aneurysms are basically spherical in shape

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16
Q

Hypothalamus

A

> Regulates homeostasis

  • Heat production
    • Chemical reactions of metabolism
    • TRH>TSH>Thyroxine>Epinephrine>
    • vasoconstriction, ↑glycolysis, ↑metabolic rates
    • SNS
    • Skeletal muscle tone, shivering, vasoconstriction
  • Heat Loss
    • Reverse the same mechanisms
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17
Q

Temperature Control: Fever

A

“Give me a fever, and I can cure any illness” – Hippocrates

  • Functions of fever:
    1) Stimulate the immune system
    2) Create an inhospitable environment for invading pathogens
  • Macrophages release endogenous pyrogen (IL-1) > PG-2 > set point increased > body is now cooler than new set point > heat generating mechanisms: shivering, vasoconstriction, TRH, etc.
  • Benefits:
    1) Increased antibody, interferon, WBC production/mobilization
    2) Increased lymphocyte recruitment to nodes
    3) Sequestered Fe
    4) Increased temp directly inhibits pathogen replication (102 to 103 is optimal)
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18
Q

Leukemia

A
  • Malignant disorders of the blood or bone marrow with uncontrolled proliferation of malignant leukocytes
  • Classification
    • Pre-dominant cell of origin
    • Degree of differentiation before becoming malignant
  • Four types
    1) ALL – Acute Lymphocytic Leukemia
    2) AML – Acute Myelogeneous Leukemia
    3) CLL – Chronic Lymphocytic Leukemia
    4) CML – Chronic Myelogeneous Leukemia
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19
Q

Acute Leukemia

A
  • Characterized by accumulation of blast cells (undifferentiated/immature cells) in the marrow that suppress normal hematopoiesis by physical overcrowding
  • Results in pancytopenia
    • Shortage of RBCs, WBCs and Platelets
  • Anemia
  • Neutropenia
  • Thrombocytopenia
  • Diseases that predispose a child to acute leukemia:
  • Down syndrome
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20
Q

Acute Lymphocytic Leukemia (ALL)

A
  • Most common type of childhood leukemia, 1/3 of all pediatric cancer
  • Incidence
    • 50
    • Down’s Syndrome (Trisomy 21)
  • B cell (85%) or T cell (15%)
    Accumulation of blast cells in the bone marrow  suppress normal hematopoiesis > physical crowding
    5 year survival rate: 80%
  • Lymphoblastic leukemia, they are dividing out of control
  • Usually B cell, rarely T
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21
Q

Bone marrow in acute lymphocytic leukemia (ALL)

A

Bone marrow aspirate from a child with B-cell Acute Lymphoblastic Leukemia. The lymphoblasts are large and have basophilic cytoplasm with prominent vacuoles.

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22
Q

Acute Myelogeneous Leukemia (AML)

A
  • Adults ~ 65 but can be any age
  • Incidence increases with age
  • Increased M vs. F
  • Idiopathic
  • Prior chemotherapy or radiation
  • Exposure to chemicals (benzene)

Auer rods - abnormal, red-staining, rod-like granule inclusions

  • Myeloblast problem
  • Usually older adults
23
Q

s/s of chronic leukemia

A
  • Progresses more slowly; permits greater numbers of mature, functional, normal cells to be produced
  • Often asymptomatic (20% have no S/S on Dx)
  • Fatigue, anorexia, splenomegaly, night sweats, low fever
  • Leukemic cells infiltrate liver, lymph nodes, spleen
  • S/S of Anemia
  • cells are not necessarily blast cells they will be further down the line
  • known as smoldering leukemias
  • s/s are not specific, a person might not even be aware of them
24
Q

Chronic Lymphocytic Leukemia (CLL)

A
  • The most common leukemia in adults
  • Incidence usually > 40
  • Cause under research
  • B Cell origin
  • Suppression of Ab production so risk of infections increases
  • Poor prognosis
  • Smudge cells or basket cells are leukocytes that have been damaged during preparation of the peripheral blood smear. This usually occurs due to the fragility of the cell. They are usually seen in chronic lymphocytic leukemia (CLL).
  • under microscope they are called smudge cells, very fragile
25
Q

Chronic Myelogenous Leukemia (CML)

A
  • Adults (25 – 60 yo)
  • 95% of cases - Philadelphia chromosome
    • Transposition of chromosomes 9 and 22
    • Radiation – cancer treatment and wars
  • Insidious onset
    1) Chronic Phase > most patients, milder symptoms (4-5 years in untreated pts)
    2) Accelerated Phase > increased blast cells, splenomegaly (hard to control WBC levels with normal chemotherapy)
    3) Blast Crisis Phase > increased blast cells, anemia, thrombocytopenia, neutropenia (resembles AML at this point >30% blast cells)
  • Myeloblast origin
  • huge age range
26
Q

Diagnosis of leukemias

A
  • CBC
    • Blasts seen in smear
  • PT/PTT - prothrombin time & partial thromboplastin time
    • Clotting time/factors
  • Bone marrow aspirate and biopsy
    • Staging and grading
  • X-ray and CT – enlarged lymph nodes in chest

*Every single one has its own classification system for its own diagnosis

27
Q

Lymphoma, what is it?

A

Cancer of the lymphocytes in the lymph nodes.

28
Q

Hodgkin’s Lymphoma

A
  • B cell lymphoma
  • High cure rate: 5 year survival rate: 83%
  • Causes
    • Most common in young adults
    • 2 peaks: 30-40 & 60-70
    • FHx, Epstein-Barr Virus
    • Family history
  • Signs and Symptoms
    • Painless lymphadenopathy: disease of the lymph node, if the lymph node hurts and you can move it under the skin you are generally good. If they don’t hurt and are fixated that is a bad sign
    • All other leukemia S/S discussed
    • Reed-Sternberg cells
      Cells look like owl eyes in their slides
  • Good cure rate
  • Find this in young adults
  • Family history is big in this disease
29
Q

False aneurysm is?

A

An extravascular hematoma that communicates w/the intravascular space. A common cause of this type of lesion is a leak between a vascular graft and a natural artery

30
Q

where do most aortas happen?

A

The aorta is susceptible to aneurysm formation because of constant stress on the vessel wall and the absence of penetrating vasa vasorum in the media layer

  • 3/4ths of all aneurysms occur in the abd aorta
  • atherosclerosis is the most common cause of arterial aneurysms because plaque formation erodes the vessel wall contributes to inflammation & release of proteinases that can further weaken the vessel
  • Hypertension also contributes to aneurysm formation by increasing wall stress
  • collagen-vascular disorders, syphilis, & other infections that affect arterial walls also can cause aneurysms
31
Q

Cardiac aneurysms most commonly form after?

A

Myocardial infarction when intraventricular tension stretches the noncontracting infarcted muscle. The stretching produces infarct expansion, a weak & thin layer of necrotic muscle, & fibrous tissue that bulges w/each systole

32
Q

Clinical manifestations for aneurysms

A
  • Depends upon where it is located
  • Aortic aneurysms often asymptomatic until ruptured, then can cause severe pain & hypotension
  • Thoracic aortic aneurysms can cause dysphagia (difficulty swallowing) & dyspnea (breathlessness)
  • An aneurysms that impairs flow to an extremity causes symptoms of ischemia
  • Cerebral aneurysms, which often occur in the circle of Willis, are associated w/S/S of stroke occur when cerebral aneurysms leak
  • Aneurysms in the heart present w/dysrhythmias, heart failure, and embolism of clots to the brain or other vital organs
33
Q

Aortic aneurysms can be complicated by the acute aortic syndromes, which include

A

Aortic dissection, hemorrhage into the vessel wall, or vessel rupture . Dissection of the layers of the arterial wall occurs when there is a tear in the intima and blood enters the wall of the artery. Dissection involves

34
Q

Common s/s of leukemia

A

1) Systemic:
- weight loss
- fever
- frequent infections
2) Lungs:
- easy SOB (because RBC’s and platelet cells are made in bone marrow, not enough RBC’s to carry O2)
3) Muscular:
- weakness
4) Bones or joints:
- pain or tenderness
5) Psychological:
- fatigue
- loss of appetite
6) Lymph nodes
- swelling
7) Spleen and/or liver:
- enlargement
8) Skin:
- night sweats
- easy bleeding and bruising (not enough platelets)
- purplish patches or spots

*WBC’s aren’t fighting infection because they don’t have any disease fighting abilities

35
Q

Symptoms of acute leukemia

A
  • Anemia: fatigue, pallor
  • Neutropenia: fever, infections
  • Thromobytopenia: petechiae, ecchymoses, epistaxis
  • Night sweats
  • Clotting Disorders: bleeding
  • Bone pain
  • Lymphadenopathy
  • Hepatosplenomegaly: upper quadrant fullness
  • DIC
36
Q

Non-Hodgkin lymphoma (other B-cell neoplasms)

A
  • B-cell (90%)
  • 14 different types – can be fast or slow growing
  • Worse prognosis than Hodgkin’s lymphoma
    • 5 year survival rate: 59%
    • B-Symptoms: Fever, weight loss, night sweats
      • Indicates disease is more wide-spread
      • Worse prognosis
  • Tx:
    • Rituximab: Commercial Ab that attacks B Cell antigen
    • antibody treatments

-the more s/s you have the generally worse the disease is

37
Q

Burkitt’s Lymphoma

A
  • B cell lymphoma
  • Causes
    • EBV (Epstein Barr Virus)
  • Signs and Symptoms
    • Tumors manifest at extranodal sites
      • African BL: mass involving the maxilla or mandible (most common)
      • Sporadic BL: mass in abdominal organs. rare
  • Testing
    • Biopsy: “Starry sky” pattern

-two types, more common one is the facial region, abdominal region is very rare

38
Q

Multiple Myeloma

A
  • Plasma cell neoplasm > involvement of the skeleton at different sites
  • Causes
    • Idiopathic
    • Possible chromosome 13 deletion (50% of cases)
    • Link to infection by Human Herpes Virus 8 (HHV-8)
      -Kaposi’s sarcoma – HHV-8
  • Signs and Symptoms
    • Incidence > men
    • Peak age 50-60
    • Suppression humoral immunity > recurrent infections
      -Why is the humoral immunity suppressed?
    • Anemia
    • Hypercalcemia – confusion, weakness, lethargy, constipation, punched out lesions > pathological fractures
      In multiple myeloma patients, the primary cause of the hypercalcemia is widespread tumor-induced bone destruction. This is primarily due to increased osteoclastic bone resorption caused by potent cytokines expressed or secreted locally by the myeloma cells (receptor activator of nuclear factor-κB ligand [RANKL], macrophage inflammatory protein [MIP]-1α, and tumor necrosis factors [TNFs]
  • plasma cells make antibodies
  • this cancer spues out antibodies but they are not normal functioning ones
  • usually older guys get this
  • person could be hypercalcemia, if you do an x ray you would see bone loss/absorption/breakdown
  • RANKL stimulates osteoclast activity which breaks down bone tissue
39
Q

Multiple Myeloma

A
  • M-protein
    • Most prominent protein in the blood - monoclonal proliferation of plasma cells in the bone marrow, meaning that there are a high number of malignant plasma cells that all originated from the same initial cell - secreting exactly the same form of immunoglobulin
    • Due to large number of malignant plasma cells
  • Bence Jones protein (80% of cases)
    • Frequently found
    • Immunoglobulin light chain found in blood and urine
    • Contributes to damage of renal tubular cells
  • PUNCHED OUT LESIONS on X-RAY
40
Q

Rheumatic Fever

A
  • Inflammatory Disorder
  • Cause
    • Strep throat (Only 3% will acquire acute rheumatic fever)
      Group A Beta-hemolytic streptococcus
      Delayed exaggerated immune response
  • Signs and Symptoms
    • Endocarditis: Heart valves (mitral) – STERILE VEGETATIONS. It’s inflammation or damage of the valve
    • Migratory, polyarthritis (moving, lots of joints. will present with joint pain at various sites on the body)
    • Chorea: Jerking muscle twitches
    • Erythema Marginatum – never on hands/face
      -Mistaken for ringworm
  • Testing
    • Rapid Strep
    • ASO – Antistreptolysin O titer (in their blood)
    • CBC
  • severity differs from person to person
  • STERILE VEGETATIONS not bacterial infection
  • 4 types of hypersensitive reactions
41
Q

Pericarditis

A
  • Inflammation of the pericardium
  • Cause
    • Viral (90%), MI, AI, Trauma
  • Signs and Symptoms
    • Acute onset chest pain, Dyspnea, Low grade fever, Feeling sick
    • Pain may radiate to the back – phrenic nerve irritation
    • Pericardial effusion > FRICTION RUB (~85% present) “sand paper sound”
  • Testing
    • EKG (PR segment depression, ST elevation without Q waves), Echocardiogram, CT, CBC
  • TX: Anti-inflammatories, Colchicine, Aspiration may be necessary
  • Most are viral & often times you don’t know which virus
  • If pericardial sac is inflamed it will create pain
  • Can make a secretion, a water secretion called a fusion
  • ST elevation is not specific
42
Q

EKG Review for pericarditis

A

Pericarditis: Depressed PR segment, diffuse ST segment elevation without Q wave

43
Q

Infective Endocarditits

A
  • Infection of endocardium – usually Streptococci or Staphylococci
  • Cause
    • Poor dental health > dental procedures, flossing, infection
    • Indwelling > catheters > IV, Foley
    • IV drug use
    • Artificial heart valves
    • Previously damaged heart valve (i.e. Rheumatic Fever)
  • Signs and Symptoms
    • Infectious symptoms, new onset murmur, arthritis symptoms, SOB, cough, edema
  • Testing
    • CBC, BC, EKG, Echocardiogram

-Cause: previously damaged heart valve
Murmer=abnormal flow across the heart valve

44
Q

Pleurisy & Pleural Empyema

A
  • Inflammation of the pleura
  • Infection in pleural space
  • Cause
    • Viral, Bacterial, AI, TB, PE
  • Signs and Symptoms
    • SOB, Chest pain increase with respiration
    • Infectious symptoms
  • Testing
    • CXR, BC, CBC, Thoracocentisis

-Old man bending down to pick up paper and he is holding his back because it hurts and it hurts to breath (story)
How to get stuff out of pleural space? Put a tube in and drain it, its called a thoracentisis

45
Q

HIV/AIDS

A
  • Immunodeficiency > RNA virus
  • Cause
    • STD, Blood, Maternal, Equipment
  • Signs and Symptoms
    • 2-4 weeks > Fever, Sore throat, lymphadenopathy, rash
      Chronic > Weight loss, diarrhea, cough, opportunistic infections, night sweats
  • Testing
    • ELISA, Western Blot, Rapid HIV test
46
Q

HIV/AIDS Statistics In US

A 
1) End of 2006
~ 1.1 million persons in the United States were living with diagnosed or undiagnosed HIV infection
2) In 2007
42,655 new cases of HIV/AIDS in adults, adolescents, and children
~ 11,000 AZ
3) High Risk Transmission
- Male – Male 
- High risk heterosexual 
- IV drug use
4) Sex
- Males 74%
- Females 26%
5) Race/Ethnicity
- African American 
- Caucasian
- Hispanic
6) Age
- 40-49 – fastest growing group
47
Q

Sepsis

A
  • Massive inflammatory response to trigger systemic inflammatory response syndrome (SIRS)
  • Cause
    • Bacterial/Viral > release of toxins
  • Signs and Symptoms
    • Fever, Tachycardia, Tachypnea, Diarrhea, ALOC, Hypotension, U/O
    • Risk > DIC, ARDS
  • Testing
    • CBC, BC, ABG, CMP, UA
  • Usually bacterial. Some type of toxin that bacteria makes is what causes it
  • Plasma portion of blood and cells should stay in but this can cause this to become leaky
  • Sepsis can progress to DIC & ARDS
  • CBC will see high WBC
  • BC-want to find out what nasty is growing in blood and know antibiotics
  • ABG- might show alkolotic because they are breathing quickly or acidosis, know which ones
  • can go to ARDS a lung problem. Capillary in lungs can become leaky
48
Q

Toxic shock syndrome

A
  • Life threatening bacterial infection
  • Cause
    • Staph aureus
    • Group A beta hemolytic strep
    • Tampons, contraceptive sponges/diaphragm
    • Wounds
  • Signs and Symptoms
    • Sudden onset > high fever, hypotension, V/D, Rash, ALOC
  • Testing
    • CBC, BC, C&S

-Clue: HIV was not around during civil war, AIDS didn’t show up until later. EXAM

49
Q

Syphilis

A
  • Infections with Treponema pallidum: STD, Childbirth, Transfusion
  • Primary
    • Painless chancre at site of transmission 10-90 day incubation period
    • Lymphadenopathy
  • Secondary (3-6 wks after sore appears)
    • Non- itchy rash on body, palms and soles
    • Feeling “ill”
  • Latent (About 1 year after infection)
    • Bacteria remain inactive in the lymph nodes and the spleen
    • Can last 3–30 years and may or may not progress to the final, or tertiary, syphilis
  • Tertiary
    • Systemic > Cardiac, CNS gummas (soft, non-cancerous growth resulting from the tertiary stage of syphilis. It is a form of granuloma. Gummas are most commonly found in the liver, but can also be found in brain, heart, skin, bone, testis)
  • Pregnancy
    • Can be transmitted during pregnancy and childbirth
  • Testing
    • RPR – Rapid Plasma Reagin Test (can test asymptomatic people), spirochetes under dark-field microscopy

-Easily treated
-it doesn’t hurt early on
Spiral shaped bacteria
w/in 10 they will get
The photos show primary, secondary, tertiary stage
RPR is a blood test you can do, you can sample blood and look for spirochetes

50
Q

Syphilis Stages

A

1) First 5 years
- no s/s are observed
2) Primary stage
- Sore/chancre found in genital area; inner part of vagina in women, penis for men
- Chancres do not result in pain and will disappear w/out treatment
3) Secondary stage
- Skin rash-rough, red or reddish brown spots on palms of hands and bottoms of feet
- Mucous membrane lesions throughout body w/out ichiness
- Fever, sore throat, headache, swollen gland, weight loss,muscle ache, fatigue
4) Tertiary stage
- Blood vessels, cardiac, nerve system problems
- damaged internal organs
- death cases
5) Latent stage
- symptoms disappear for 1-20 years
- diagnosis through blood testing
- relapse symptoms

51
Q

False aneurysm is?

A

An extravascular hematoma that communicates with the intravascular space. A common cause of this type of lesion is a leak between a vascular graft and a natural artery

52
Q

Why is the aorta susceptible to aneurysm formation?

A

Because of constant stress on the vessel wall and the absence of penetrating vasa vasorum in the media layer.

53
Q

Causes of aneurysms

A

1) Atherosclerosis most common cause of arterial aneurysm in abdominal wall.
2) Hypertension increases wall stress
3) Collagen-vascular disorders (Marfan syndrome), syphilis, and other infections that affect arterial walls
3) Cardiac aneurysms most commonly form after myocardial infarction
4) Smoking

54
Q

High risk for infective endocarditis

A

1) IV drug abuser
2) Male > female
3) An artificial heart valve
4) Dental work
5) Congenital heart diseases
6) Hypertrophic cardiomyopathy

Pathophysiology (22 decks)

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