Final Exam Flashcards
What happens in the ribosomes?
protein synthesis
what happens in the mitochondria?
energy production
What is aerobic energy production
energy production with O2
anaerobic energy production
- energy production without O2
- a lot less energy is produced
Should Na+ ions be higher or lower OUTSIDE of the cell
HIGHER
should K+ ions be higher or lower inside the cell
HIGHER
how does the sodium potassium pump work
- it uses energy to actively transport across cell membrane
- if the pump breaks/does not work, ions will be on the wrong side of the membrane (too much in or out of cell)
benign cells
- looks like parent cell
- cells line up in orderly fashion
- cells know when to stop growing
malignant cells
- contact inhibition
- metastasize
- grow over other things
What can result from Marfan’s syndrome?
- abnormal chest, heart, and lung problems
- eye problems
- short torso
- tall, thin body frame
- long arms, legs, and fingers
normal WBC level
4,000-10,000 cells/mL
leukocytosis
- high WBC
- greater than 11,000
leukopenia
- low WBC
- fewer than 4,000
Are CRP and ESR increased or decreased during inflammation?
- increased
- they are non specific markers that tell us if there is inflammation but not where it is
What are the 5 cardinal signs of inflammation
- redness
- heat
- swelling
- pain
- loss of function
how do wounds heal properly
- hemostasis: limit blood loss
- inflammation
- proliferation, granulation tissue formation, angiogenesis, epithelization
- wound contraction and remodeling
healing by primary intention
- simple reapproximation of edges of wound
- simple reepithelialization
- best outcome of healing
- surgical incision type of healing
healing by secondary intention
- gap in the tissue
- prolonged healing involving generation of granulation tissue and more complex tissue
- scar tissue formation/deformity
healing by tertiary intention
- gap n the tissue
- contaminated wound
- temporary loose closure to allow for drainage
- firm closure of wound after decontamination
- skin graft often needed
- scar tissue/deformity
innate immunity
- born with it
- nonspecific response
- cannot be transferred
- inflammatory process is part of it
- ex. skin, cilia
acquired immunity
- get it from contact with a pathogen
- specific response to invasion
- B- cells: memory, make antibodies
- T cells: cell mediated immunity
- recognize self vs non self
How does inflammation work in immunity
- it is part of innate immunity
- immunocompetence plays an important role in immune response and risk for inflammatory response
natural active immunity
- longest lasting immunity
- person in natural world comes in contact with antigen
- your body actively makes the antibodies
artificial active immunity
- vaccines, boosters
- you artificially get the antigen but your body actively makes the antibody
- not as long lasting but you can re up it
natural passive immunity
- mom to baby
- mom’s body makes the antibody and passes them to baby
- temporary
- given to baby through placenta or breastmilk
- when the antibody dies, baby cannot make more
artificial passive immunity
- antibody is artificially acquired
- only lasts for the life of the antibody
- given to people that are very sick
- ex. immunoglobulin infusion
type 1 hypersensitivity: immediate hypersensitivity
- B cell mediated
- hives, nasal discharge, bronchial asthma, allergic gastroenteritis
- can lead to anaphylaxis (inflammatory response so large that the airway closes, body is producing too much IgE)
- when anaphylaxis occurs STOP ALLERGEN
type 2 hypersensitivity: cytotoxic hypersensitivity
- Igs attack antigens on the cell surface
- antibody-mediated cell lysis results (bc the body wants to kill it off)
- ex. blood transfusion reaction
- s/s blood transfusion reaction: high temp, may have itchiness, BP changes, HR changes
- STOP INFUSION if any reaction occurs, do not flush
type 3 hypersensitivity: immune complex hypersensitivity
- antigen-antibody (immune) complex deposited in tissues
- tissue damage results
- may be systemic (lupus) or localized (RA)
- results in constant inflammatory response
- most of the the the antigen is unknown
type 4 hypersensitivity: delayed hypersensitivity
- previous exposure to antigen primes the T cells
- T cell attack does not occur until days after initial exposure
- ex. poison ivy, transplant rejection
where is extracellular fluid located
the bloodstream
where is intracellular fluid located
inside of cells
hydrostatic pressure
- pushing force that pushes water from ECF into ICF
oncotic pressure
- the pulling force created by albumin, which favors fluid movement from the ICF into the ECF
why is albumin important
- when you lose albumin, oncotic pressure drops and hydrostatic pressure kicks up
- in a constant inflammatory state albumin will leak out of cells
- keeps fluid in the cells
hypotonic solution
- more water than blood
- causes shift from ECF to ICF
- 0.45% NaCl
- given for dehydration, for keeping veins open
Isotonic solution
- same tonicity as blood
- no fluid shifts or change in cell size
- NaCl, Lactated ringers, D5 0.9% NaCl
- given to hydrate patients who are NPO
hypertonic solution
- more blood than water
- causes fluid to shift from ICF into ECF, draws water out of cell
- 3% NaCl, mannitol
- given for cellular edema
Why is the RAAS system activated
the kidneys want more blood because they aren’t perfusing, this causes blood pressure and blood volume to go UP
normal Na levels
135-145
normal K+ levels
3.5-5.2
normal Ca levels
8.7-10
normal PO4 levels
2.5-4.5
normal Mg++ levels
1.5-2.5
s/s hypovolemic hyponatremia
- thirst
- hypotension
- tachycardia
- neurological deficits may develop
s/s hypervolemic hyponatremia
- headache
- lethargy
- confusion
- muscle cramps
s/s hypokalemia
- anorexia
- nausea
- vomiting
- sluggish bowel
- cardiac arrhythmias
- postural hypotension
- muscle fatigue and weakness
- leg cramps
- prolonged PR interval
- flattened T waves
- digitalis toxicity
s/s hyperkalemia
- numbness
- muscle cramps all over
- diarrhea
- ECG changes
- can lead to cardiac arrest
s/s hypocalcemia
- neuromuscular excitability
- paresthesia
- hypotension
- cardiac arrhythmias
- chronic: bone pain and fragility
s/s hypercalcemia
- decreased neuromuscular excitability
- weakness
- renal calculi
- cardiac arrhythmias
s/s hypophosphatemia
- tremors
- muscle weakness
- hyporeflexia
s/s hyperphosphatemia
- same as hypocalcemia
- neuromuscular excitability
- paresthesia
- hypotension
- cardiac arrhythmias
s/s hypomagnesemia
- usually occurs in conjunction with hypocalcemia and hypokalemia
- anorexia
- nausea
- vomiting
- sluggish bowel
- cardiac arrhythmias
- postural hypotension
- muscle fatigue and weakness
- leg cramps
- prolonged PR interval
- flattened T waves
- digitalis toxicity
- neuromuscular excitability
- paresthesia
- hypotension
- cardiac arrhythmias
- chronic: bone pain and fragility
s/s hypermagnesemia
- too much neuromuscular relaxation
- muscular flaccidity
- cardiac problems
characteristics of arteries
- carry oxygenated blood AWAY from the heart
- pump blood themselves
- high pressure system
- responsible for PULSES
arteriosclerosis
hardening/narrowing of the arteries
atherosclerosis
plaque buildup in arteries
risk factors for peripheral artery disease (PAD)
- gender (men have greater risk than women)
- age
- diabetes mellitus type 2
- family hx
- tobacco use
- hypertension
- obesity
- lifestyle factors
What is the treatment for PAD?
- lifestyle modification: diet, exercise, no smoking
- medications
- peripheral arterial revascularization procedures help restore circulation
- open surgical bypass grafting
- dangle legs
what is the primary sign of PAD
intermittent claudication
characteristics of veins
- thein walled, flexible
- return “trash” blood to the heart
- rely on skeletal muscle pump and valves
- can stretch and hold a lot of fluid which can = edema
What is Virchow’s triad
- venous stasis
- vascular damage
- hypercoagulability
chronic venous insufficiency
- results from damage to deep veins in legs/ incompetent valves which causes impaired venous return
- edema d/t pooling blood
clinical presentation CVI
- thin, shiny skin
- dusky discoloration
- edema
- poor healing
- reduced/absent hair distribution
- stasis dermatitis
How do we treat CVI
- elevate legs
- wear compression stockings all the time
- SCDs
- anticoagulant or antiplatelet meds
- venoablation
normal platelet values
150,000-400,000
thrombocytopenia
- low platelet count
- less than 100,000
thrombocytosis
- high platelet count
- greater than 750,000
what is pt at risk for with platelet count too low
risk for bleeding
what is pt at risk for with platelet count too high
risk for clotting
extrinsic pathway
- activated when there is injury to the blood vessel from the outside in
- Factor 7 and tissue factor only
what lab is extrinsic pathway measured with
PT/INR
intrinsic pathway
- activated when there is injury to the blood vessel from inside out
what lab is intrinsic pathway measured with
- PTT (Play Table Tennis inside)
- the higher to PTT the higher the risk for bleeding
aspirin
- most common antiplatelet drug
- acts on platelets for the life of the platelet
warfarin
- better for venous clots
- inhibits Vitamin K
- interferes with vitamin K dependent clotting factors
- monitor with PT/INR
heparin
- better for arterial clots
- slows or stops the coagulation pathway
- monitor with PTT
- inhibits intrinsic pathway
What is DIC
- disorder of clot formation and bleeding episodes
- clot formation
- depletion of coagulation
- elevated fibrinolysis leads to bleeding
What type of patient does DIC happen in?
- critically ill
- develops secondary to other significant disorders, such as septic shock, massive trauma, burns, transfusion
how is DIC diagnosed
- elevated D-dimer
- clotting times
- RBC hemolysis
how is DIC treated
- control primary disease
- prevent further clotting
- transfuse with FFP (fresh frozen plasma)
what is pyelonephritis
- infection of renal pelvis
- ascending UTI
- stasis of urine plays a role
what is pyelonephritis caused by
- obstruction somewhere in the renal system
- urine backs up into the kidneys
s/s pyelonephritis
- fever
- abdominal or CVA tenderness
- flank pain
- dysuria
- urinary frequency
- microscopic hematuria
- pyuria (WBC in urine)
- leukocyte esterase test of urine
treatment for pyelonephritis
- abx
- analgesics if needed
- fluid intake greater than 3 L/day
- remove urological obstruction, if present
what are complications fo pyelonephritis
- chronic pyelonephritis
- which deteriorates into chronic renal insufficiency, which may develop into end stage renal disease
what is nephrolithiasis
stones in kidneys
risk factors for nephrolithiasis
- genetic susceptibility
- dehydration
- hypercalcemia
- hyperparathyroidism
- gout
- hyperuricemia
- urinary tract infection
- immobility
lower urinary tract infection
- most commonly caused by E. coli, originating from bowel
- women at higher risk
- stagnant urine increases infection risk
risk factors for lower UTI
- female
- poor hygiene
- taking baths
- BPH
- tight clothing
- dehydration
- diabetes
- sexual intercourse
- pregnancy
- bladder cancer, urinary catheterization (in men)
s/s lower UTI
- increased frequency, dysuria, and urgency
- hematuria
- fever (not always present)
s/s lower UTI
- increased frequency, dysuria, and urgency
- hematuria
- fever (not always present)
How can we prevent UTIs?
- patient education
- shower rather than bathe
- wipe from front to back
- drink liberal amounts of fluids daily to flush out bacteria, may be helpful to drink 1 glass of cranberry juice a day
- avoid fluids that are urinary tract irritants (coffee, tea, alcohol)
- void every 2-3 hours and completely empty the bladder
- take medication exactly as prescribed
- notify PCP if symptoms persist
- consult primary provider regularly for follow up
potential complications of UTIs
- urosepsis
- ascending UTI becomes pyelonephritis
chronic renal failure
- characterized by dropping GFR
- irreversible and progressive, with gradual onset
- usually progresses to ESRD
- hemodialysis or kidney transplant needed
- DM, HTN are leading causes
leading causes of CRF
- DM
- HTN
s/s CRF
- CBC, BUN, and Cr serum levels, urinalysis, albumin levels
- renal imaging studies
treatment for CRF
- fluida and electrolyte management, along with BP management
- GFR less than 10-20 mL/min- dialysis, kidney transplant evaluation
potential complications of CRF
- encephalopathy
- hyperparathyroidism
- heart failure
- infertility
- thrombocytopenia
- anemia
- electrolyte imbalance
- high BUN
- edema
is asthma obstructive or restrictive
obstructive
asthma
- hyperreactive airway disease of bronchioles
how is asthma diagnosed
PFT during an acute asthma attack
treatment for asthma
- stepwise approach
- maintenance medications: daily
- rescue: acute attack
- limit exposure to allergens, know triggers
COPD
- must have in combination chronic bronchitis and emphysema, and hyperreactive airways
- smoking is a MAJOR cause
- genetic and environmental factors
- SEVERE COPD results in Cor Pulmonale
what do alveoli look like in chronic bronchitis
shrunken alveoli
what do alveoli look like in emphysema
- distended, nonrecoiling alveoli
- alveoli lose elasticity
how is COPD diagnosed
- COPD assessment test
- PFT’s
- CBC, chest x-ray, ABG’s, ECG
how is COPD treated
- stepwise approach with medications
- smoking cessation, pulmonary rehabilitation, vaccinations
- oxygen therapy: continuous oxygen when PaO2 less than 55 mm Hg or SaO2 less than 88%
- teaching pursed lip breathing
s/s emphysema
- “pink puffer”
- SOB and scant sputum production
- thin, cachectic, rosy skin tones
- adventitious sounds are less common
- sputum is scant and like evaporated milk
- dyspnea before cough
- barrel chest
- use of accessory muscles
s/s chronic bronchitis
- “blue bloater”
- chronic, productive cough
- often overweight, obese
- rhonchi and wheezes
- copious, purulent drainage like condensed milk
- cyanotic
- peripheral edema
- ** cough 3 months of year for at least 2 years
primary pneumothorax
just happens , no underlying disease process
secondary pneumothorax
lung collapses because of underlying disease process
traumatic pneumothorax
penetrating wound to thoracic cage and pleural membrane
tension (closed) pneumothorax
closed wound that allows air into the pleural cavity but not out
iatrogenic pneumothorax
caused by any medical procedure complications, can often be a parting gift from central line insertion
how are primary, secondary, traumatic, and iatrogenic pneumothorax treated
chest tube with suction
how is a tension pneumothorax treated
needle insertion to remove air
pleural effusion
- abnormal collection of fluid in pleural space
- results of heart failure, severe pulmonary infections
- fluid can be exudate, transudate, purulent, lymph, blood
s/s pleural effusion
- dyspnea
- tachypnea
- sharp pleuritic CP
- dullness to percussion
- diminished breath sounds on affected side, maybe even absent over area of effusion
treatment for pleural effusion
thoracentesis
thoracic cage deformity
- anything that structurally makes it hard for lungs to fully inflate
- kyphosis, scoliosis
treatment for cage deformity
orthopedic brace
pulmonary fibrosis
- may be idiopathic: repeated injury to the alveoli that we do not know the cause is
- may be caused by environmental particles like coal, dust, asbestos, silica, anthrax
- fibrotic changes decrease lung compliance, lungs become stiff because of repeated inflammation to the alveoli
s/s pulmonary fibrosis
- dyspnea
- tachypnea
- crackles
- eventual cyanosis
- CXR results in “ground glass” appearance
treatment for pulmonary fibrosis
- try to decrease inflammation/inflammatory response
- may treat with O2
- bronchodilators, corticosteroids
pulmonary edema
- edema in the pulmonary veins
- often caused by heart failure
- blood backs up into the veins of the lungs and increases pressure
- when the pressure is too great, fluid is pushed in to the alveoli of the lungs
pulmonary embolism
DVT dislodges and travels to lungs
pulmonary hypertension
- high blood pressure that affects arteries in the lungs, right side of heart, walls of pulmonary arteries become thick and stiff and cannot expand very well to allow proper blood flow
what is ARDS
- adult respiratory distress syndrome
- injury to alveoli, pulmonary capillaries causes sudden, progressive pulmonary edema called flash pulmonary edema
- arterial hypoxemia does not improve with administration of O2
who is at risk for ARDS
- critically ill patients
- sepsis
- trauma
- massive transfusions
- acute pancreatitis, aspiration
what does ARDS require
- intubation, sedation, and mechanical ventilation
- death is common
Crohn’s disease
- lesions can be anywhere gum to bum
- skip lesions
- cobblestone appearance
- RLQ abdominal pain
What is a potential complication of Crohn’s disease
toxic megacolon
ulcerative colitis
- involves large intestine only
- isolated to the colon and rectum
- ulceration is continuous
- LLQ abdominal pain
- bleeding often occurs
GERD
- problem with tone of LES
- regurgitation of stomach acid into esophagus
selye’s stress response theory
- alarm
- resistance
- exhaustion
binge eating
when you just keep eating with no intention of getting rid of food (like inducing vomiting)
effects of immobility
- atelectasis
- bone demineralization
- muscle deconditioning
- decubitus ulcers
- depression
- decreased GI motility
- kidney stones
- decreased pulmonary function
- UTI
- venous stasis
metabolic alkalosis
- vomiting
- diarrhea
- NG tube suction
- low K+
- low Ca
Tx: treat underlying cause
metabolic acidosis
- diabetics and ketoacidosis
- high K+
- high Ca
- Tx: treat underlying cause
respiratory alkalosis
- breathing too much CO2 off
- hyperventilation
- high RR
- panic attack
- breath into paper bag
respiratory acidosis
- holding onto CO2
- overdose
- low RR
normal pH levels
7.35-7.45
normal PCO2 levels
35-45
normal bicarb levels
22-26
fasting blood glucose level for diabetes diagnosis
126 or greater
OGTT result for diabetes
200 or greater
random glucose level for diabetes diagnosis
200 or greater
A1C level for diabetes diagnosis
6.5% or higher
what will urinalysis show in diabetes
- ketones
- glucose
hyperglycemia cause
- stress
- illness
- eating too much
- dehydration
- lack of exercise
s/s hyperglycemia
- polydipsia
- polyuria
- polyphagia
- blurred vision
- electrolyte imbalances
treatment for hyperglycemia
- reverse process
- give insulin
hypoglycemia cause
- taking too much insulin
- not eating enough carbs
- strenuous exercise
hypoglycemia s/s
- sweating
- hunger
- dizziness
- nervousness
- tremulousness
- irritability
- headache
- heart palpitations
- confusion
- disorientation
- inability to concentrate
- seizures
- stupor or loss of consciousness
- blurred vision
hypoglycemia treatment
- if awake: EAT, foods high in SUGAR
- if asleep: inject DEXTROSE
what does the anterior pituitary secrete
- growth hormone
- adrenocorticotropic hormone
- TSH
- FSH
- LH
- prolactin
what does the posterior pituitary secrete
- oxytocin
- ADH
what does thyroid control
METABOLISM
hypothyroidism
- couch potato
- hypercholesterolemia
- gains wt easily
- decreased fertility
- delayed reflexes
- sluggishness
- feeling cold
- constipation
- lethargy
- fatigue
hyperthyroidism
- hyperdrive
- anxiety
- tremor
- tachycardia
- feeling warm
- wt loss
- exophthalmos
- atrial fibrillation
- decreased fertility
which electrolyte goes with parathyroid
calcium and albumin
SIADH
- holding onto water
- excess ADH
- tells kidneys not to diurese
s/s SIADH
- same as fluid overload
- hypertension
- swelling
- SOB
DI
- insufficient ADH
- kidneys are not told to stop diuresing so you get rid of all your fluid
s/s DI
- same as dehydration
- hypotension
- dry mouth
- feeling thirsty
- fatigue
- dark urine
diagnostics for SIADH and DI
check adh levels
treatment for SIADH and DI
fix underlying cause- pituitary
Addison’s disease
- adrenal insufficiency
- low sodium
- everything low
s/s addisons
- tan skin
- weight loss
- fatigue
- muscle weakness
- light headed
Cushing’s
- too much cortisol
- immune system depressed
s/s cushings
- wt gain
- neck fat/humpback
- moon facies
- easy bruising
- striae
- muscle weakness
end organ examples
- bones
- adrenal cortex
- adrenal medulla
- thyroid
- parathyroid
- testes/ovaries
- mammary glands
- uterus
- kidneys
