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NURS3303 FINAL EXAM!!! QUESTIONS WITH
100% ACCURATE ANSWERS
CELLULAR BIOLOGY - ANSWER
Energy Production - ANSWER The stages of cellular respiration include glycolysis, pyruvate oxidation, the citric acid or Krebs cycle, and oxidative phosphorylation. What organelle produces ATP (energy)? - ANSWER Mitochondria INFECTION AND INFLAMMATION - ANSWER Infection phases - ANSWER - INCUBATION PERIOD- Period of infection before symptoms appear
- PRODROMAL PERIOD- Is when the patient just doesn't feel good/right
- ACUTE PHASE- This is when it is a full blown infection (sometimes asymptomatic) ā The length of the acute phase depends on the virulence and host resistance
- RECOVERY PHASE- What are some clinical Signs/Symptoms of infection? - ANSWER LOCAL- Redness, swelling, heat, pain/tenderness, purulent exudate, swollen lymph nodes SYSTEMIC- SIGNS: Elevated WBC>10,000 and left shift (increased neutrophils). SYMPTOMS: Fever, fatigue, anorexia, headache, muscle aches, seizures, disorientation or loss of consciousness What types of transmission are there? Examples? - ANSWER - Direct contact
- Indirect contact
- Droplet contact
- Vector borne
- Blood-blood transmission-> Blood transfusion is the most common method of transmission of bloodborne infections o Needlestick or lacerating injury with a sharp instrument contaminated with infected blood o Intravenous drug users can contract infection from unsterile needles o Bloodborne pathogens can also enter the body via the eye, naso-oral mucous membranes, and skin that is not intact
CHAIN OF INFECTION
How do we break the chain of infection? - ANSWER Infectious agents Resevoir Portals of Entry Modes of Transmission Portals of Exit Susceptible host By washing hands, wearing PPE, disinfecting surfaces/equipment Inflammation
- S/S?
- Labs? - ANSWER A protective, coordinated response of the body to an injurious agent
- It involves a specific sequential reaction to cell injury
- Inflammation is NOT the same as infection. You can have inflammation without infection, but you cannot have infection without causing inflammation
- GOAL: To wall off the area of injury, prevent spread of the injurious agent, and bring the body's defenses to the region under attack CARDINAL SIGNS:
- Redness
- Swelling
- Warmth
- Pain
- Loss of function S/S:
- LOCAL- Heat, Erythema (redness), Pain, Edema, Loss of function
- SYSTEMIC- Fever, Leukocytosis (increased # of WBCs), Nonspecific symptoms (such as Malaise, Headache, and Anorexia) PHASES:
- Vascular Phase
- You get it by receiving antibodies from another source Ex: breast milk, IgG for Hepatitis exposure, Covid antibody administration Passive acquired is natural through placenta and breast milk Passive artificial is through injection of immunoglobulins or anti toxins(ex: rabies vaccine) Active Acquired Immunity - ANSWER - Long term immunity
- You get Active acquired by either having the disease or getting the vaccine (through exposure to antigen) Ex: vaccines
Humoral Immunity - ANSWER - B cell response/immunity --Involves antibodies (produced by plasma B cells) -- Effective against pathogens outside the cell -- Mature when exposed to antigens -- Assisted by CD4 helper cells --B cells are less effective against viruses than other microorganisms because viruses get inside the cell
CELLS
- Plasma B cells
- Memory B cells
Cell-mediated Immunity - ANSWER T-cell response --Effective against pathogens inside the cell --Stimulated by APC cells CELLS
- CD4 Helper T cells influence ALL immune cells
- CD8 Cytotoxic T cells directly attack antigens
How do vaccines work? What type of immunity is this? - ANSWER - Vaccines contain weakened or inactive parts of a particular organism (antigen) that triggers an immune response within the body
Immunodeficiency - ANSWER aka immunocompromisation
- a state in which the immune system's ability to fight infectious diseases and cancer is compromised or entirely absent.
HIV - ANSWER HIV (Human Immunodeficiency Virus) causes AIDS and interferes with the body's ability to fight infections.
PATHO PROCESS-
- the virus inserts DNA into the CD4 cells
- Viral RNA is reverse transcribed into DNA and inserted into host CD4 genome
- CD4 cell becomes a factory of HIV viral particles
- Release into surrounding tissue
budding of viral particles
- If CD4 cells are inactive, the virus will lie dormant until cell replicates
PATHO-
- T helper cells dysfunction- CD4 cells
- Loss of B cell and T cell activation (humoral and cell mediated immunity impacted)
- Destroys macrophages- damages innate immune response (which is why opportunistic infections and cancer are common in HIV patients)
- Decreases chemotaxis, interleukin production, and antibody production
- Impaired cytotoxic activity
- Impaired antigen presentation
antibodies against the body's own tissues Ex: SLE,
Hypersensitivity Reactions
- Types? - ANSWER Type 1 (immediate hypersensitivity)
Type 2 (Cytotoxic)--Blood transfusion rejection
Type 3 (Immune Complex)
Type 4 (Cell mediated or Delayed Hypersensitivity)--Transplant Rejection
Type 1 hypersensitivity - ANSWER - Allergic or atopic disorder
- Local or systemic disorder
PROCESS
- IgE antibodies bind to mast cells
- Mast cells degranulate (this causes the release of histamine--> which increases capillary permeability and vasodilation)
RESULTS (depends on portal of entry)
- Mucous membranes: swelling, increased mucous production
- Skin: redness, vesicles, itching
- Bronchioles: swelling, constriction
EXAMPLES
- hives
- atopic dermatitis (eczema)
- allergic rhinitis
Can cause Anaphylaxis
Type 2 hypersensitivity - ANSWER - Cytotoxic Reactions
- BLOOD TRANSFUSION REACTIONS due to ABO incompatibilities (not matching blood types)
PROCESS
- antibodies attack antigens on donor cells
RESULTS
- both cells destroyed- hemolysis
Ex: Hemolytic Transfusion Reaction
- when you give a patient the wrong type of blood
Type 3 hypersensitivity - ANSWER - Immune Complex
PROCESS
- antigen-antibody molecule imbeds in tissue
RESULTS
- damaged and scarred tissues
- decreased function in scarred tissue
- ANEMIA causes a Reduction In Oxygen Transport To Tissue
GENERAL SIGNS/SYMPTOMS:
- pallor of skin, nailbeds, conjunctiva
- excessive fatigue
- weakness and feeling "faint"
- shortness of breath with exertion
- exercise intolerance
- chest pain
- tachycardia
- nutritional anemias: sores in mouth, swollen cracked lips, glossitis(inflammation of the tongue)
- impaired healing
- foggy thinking (due to hypoxia-not enough oxygen getting to the brain)
TYPES: iron deficiency, pernicious(B12), hemolytic, acute/chronic blood loss,
What is the most common type of anemia? - ANSWER iron deficiency anemia
How are blood cells formed? How are they differentiated? - ANSWER Blood cells develop from hematopoietic stem cells and are formed in the bone marrow through the highly regulated process of hematopoiesis. Hematopoietic stem cells are capable of transforming into red blood cells, white blood cells, and platelets.
- Two types of white blood cells, T and B cells (lymphocytes), are also produced in the lymph nodes and spleen, and T cells are produced and mature in the thymus gland.
Neoplasms (blood and lymph theory) - ANSWER
When do clots form? - ANSWER - when blood flow is sluggish or stagnant (often in the extremities)
- when blood vessel walls are damaged
- when body is injured
Clotting abnormalities - ANSWER HYPERCOAGULABILITY: Increased Clotting
- Increased platelets (thrombocytosis)= increased risk of clot formation
- Cause: splenectomy, leukemia, polycythemia
- Stasis of blood- activates coagulation system by increasing pro-coagulation factors OR decreasing anti-coagulation factors
High risk of venous thrombus in legs- Deep Venous Thrombus (DVT)
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): A disorder of both clot formation and bleeding episodes in critically ill patients
Clotting happens first- fibrin deposits in blood vessels- destroys organs/tissue Consumes clotting factors- consumptive disorder Occurs in 30-50% of septic patients It is very severe and very hard to treat
(the patient forms clots that block arteries, once clotting factors are used up the patient starts to hemorrhage)
CARDIOVASCULAR - ANSWER
- Troponin (if troponin is >0.2, it means there is MI)
- CRP
- CK-MB EKG changes
COMPLICATIONS:
- Dead heart muscle can NOT beat!! (reduced contractility)
- Electrical conduction cannot pass through dead tissue--> irregular heart rhythms (dysrhythmias)
- Papillary muscle rupture
- Thromboembolism
- Pericarditis (inflammation around heart)
- Heart failure (heart muscle remodels)
TYPES: STEMI
- ST elevated MI
- seen on EKG.
- Worst type
- full thickness damage to myocardium, due to complete occlusion of major coronary artery (usually LAD)
NSTEMI
- Non ST E levated MI
- T segment elevation does not appear
- due to partial occlusion of coronary artery.
Angina - ANSWER chest pain due to reduced blood flow to the heart
- Stable Angina: chest pain with stress, exercise, exertion (pain goes away with rest)
- Unstable Angina: unpredictable chest pain; happens even at rest (pain does not go away with rest)
- Angina Pectoris: chest pain due to myocardial ischemia. More severe with exercise, treated with NTG, rest
- Unstable Angina: new onset chest pain or increasing frequency or intensity of pain in a client with known angina. Indication of ischemia myocardium. Worse with exercise.
Right heart failure - ANSWER PATHO: Right sided HF is MOST COMMONLY CAUSED BY LUNG DISEASE. When the right ventricle fails, it is unable to pump the blood received from the body. Pooling of this blood causes peripheral edema, hepatosplenomegaly, and jugular vein distention. The right ventricle may fail because of pulmonary disorders causing reduced oxygenation. Low oxygen in the lungs causes vasoconstriction, increasing the afterload the right ventricle works against. This process is known as cor pulmonale.
SYMPTOMS:
- fatigue
- increased peripheral venous pressure
- ascites
- enlarged spleen and liver
- may be secondary to Chronic Pulmonary Problems
- jugular vein distention
- anorexia/GI distress
- weight gain
- dependent edema (in legs)
- weak peripheral pulses
- cardiomegaly
- paroxysmal nocturnal dyspnea
- increased PCWP (pulmonary capillary wedge pressure)
- cough
- wheezes
- crackles
- frothy or blood tinged sputum
- restlessness
- confusion
- orthopnea
- tachycardia
- exertional dyspnea *Many of the signs and symptoms are due to the body's compensation.
EFFECTS: Backward (causes LUNG problems--> think Left= Lung)
- increases hydrostatic pressure in Left atrium
- increases pressure in pulmonary vein-->causes pulmonary edema
- increases pressure in pulmonary capillaries
Forward
- decreased output to major organs
PROCESS OF EFFECTS:
- Left ventricle weakens and cannot empty
- Decreased Cardiac Output to system
- Decreased blood flow to kidneys stimulates RAAS (forward effect)--> leads to increase in blood volume therefore an increase in BP
- There is back flow of blood into the pulmonary vein
- High pressure in pulmonary capillaries leads to pulmonary edema
COMPENSATORY MECHANISMS: Baroreceptors detect low blood pressure and respond by increasing heart rate. Anti-diurectic hormone, abbreviated ADH, is released to increase blood
Treatment of Heart Failure - ANSWER Goal: -Reduce volume/preload -Increase contractility -Reduce resistance/afterload
Many medications treat heart failure and its compensations.
- Diuretics increase urine output and remove excess fluid volume
- Inotropic agents stimulate more forceful contractions - ACE inhibitors reduce fluid volume and afterload
- Beta blockers help to slow the heart rate and reduce afterload.
Atherosclerosis - ANSWER WHAT?: hardening of the arteries by the accumulation of fatty deposits (plaque)
RISK FACTORS:
- high cholesterol
- triglyceride levels
- high blood pressure
- smoking
- diabetes
-stress -Smoking!! (nicotine is a vasoconstrictor)
PATHO: Effects
- creates a high shearing horse that damages endothelial linings of arteries (arteries most affected are in the retina, brain, lower extremities, and the renal artery)
- increases resistance against the hearts left ventricle causing excessive workload on the heart and left ventricular hypertrophy (An enlarged cardiac muscle requires more O2 and increased circulation--increases the risk of Myocardial ischemia, infarction, and heart failure)
Increased PVR --> Reduces system capacity --> Increases Cardiac Workload --> Decreases blood flow --> Decreased blood flow to kidneys --> RAAS activation --> Increased vasoconstriction --> Increased PVR --> continuation of cycle
LONG-TERM EFFECTS: Heart pump failure (Decreased CO)
- renal failure
- heart failure Damage to arterial walls
- hemorrhagic stroke
- weakens arterial walls--> aneurysms Sclerotic (hard) arteries and narrowed lumen Decreased blood flow
- ischemia organs/peripheral vessels
- infarction
- retinal damage--> Blindness
- hypertensive encephalopathy
- cerebral hemorrhage--> Stroke
ORGANS MOST AFFECTED BY HTN: -Heart -Retina -Kidneys -Brain -Lower extremities
Shock - ANSWER Shock is a state of cardiovascular collapse (regardless of the type)--There is NOT an adequate amount of blood in circulation--so there is reduced perfusion to organs
TYPES:
- Hypovolemic
- Cardiogenic
- Vasogenic/Neurogenic
- Septic
- Anaphylactic ALL TYPES OF SHOCK CAUSE CELLULAR HYPOXIA WHICH LEADS TO NEED FOR ANAEROBIC METABOLISM LEADING TO ACIDOSIS!!!
STAGES OF SHOCK: Initial Phase
- BP drops--> Sympathetic NS and RAAS stimulated--peripheral vasoconstriction and increase blood volume
- Significant reduction in tissue perfusion Progressive Stage:
- Blood shunted to brain/heart--ischemia of major organs occurs--affects lungs, kidneys,
