Final Exam Flashcards
1
Q
What happens in the ribosomes?
A
protein synthesis
2
Q
what happens in the mitochondria?
A
energy production
3
Q
What is aerobic energy production
A
energy production with O2
4
Q
anaerobic energy production
A
- energy production without O2
- a lot less energy is produced
5
Q
Should Na+ ions be higher or lower OUTSIDE of the cell
A
HIGHER
6
Q
should K+ ions be higher or lower inside the cell
A
HIGHER
7
Q
how does the sodium potassium pump work
A
- 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)
8
Q
benign cells
A
- looks like parent cell
- cells line up in orderly fashion
- cells know when to stop growing
9
Q
malignant cells
A
- contact inhibition
- metastasize
- grow over other things
10
Q
What can result from Marfan’s syndrome?
A
- abnormal chest, heart, and lung problems
- eye problems
- short torso
- tall, thin body frame
- long arms, legs, and fingers
11
Q
normal WBC level
A
4,000-10,000 cells/mL
12
Q
leukocytosis
A
- high WBC
- greater than 11,000
13
Q
leukopenia
A
- low WBC
- fewer than 4,000
14
Q
Are CRP and ESR increased or decreased during inflammation?
A
- increased
- they are non specific markers that tell us if there is inflammation but not where it is
15
Q
What are the 5 cardinal signs of inflammation
A
- redness
- heat
- swelling
- pain
- loss of function
16
Q
how do wounds heal properly
A
- hemostasis: limit blood loss
- inflammation
- proliferation, granulation tissue formation, angiogenesis, epithelization
- wound contraction and remodeling
17
Q
healing by primary intention
A
- simple reapproximation of edges of wound
- simple reepithelialization
- best outcome of healing
- surgical incision type of healing
18
Q
healing by secondary intention
A
- gap in the tissue
- prolonged healing involving generation of granulation tissue and more complex tissue
- scar tissue formation/deformity
19
Q
healing by tertiary intention
A
- 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
20
Q
innate immunity
A
- born with it
- nonspecific response
- cannot be transferred
- inflammatory process is part of it
- ex. skin, cilia
21
Q
acquired immunity
A
- 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
22
Q
How does inflammation work in immunity
A
- it is part of innate immunity
- immunocompetence plays an important role in immune response and risk for inflammatory response
23
Q
natural active immunity
A
- longest lasting immunity
- person in natural world comes in contact with antigen
- your body actively makes the antibodies
24
Q
artificial active immunity
A
- vaccines, boosters
- you artificially get the antigen but your body actively makes the antibody
- not as long lasting but you can re up it
25
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
26
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
27
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
28
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
29
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
30
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
31
where is extracellular fluid located
the bloodstream
32
where is intracellular fluid located
inside of cells
33
hydrostatic pressure
- pushing force that pushes water from ECF into ICF
34
oncotic pressure
- the pulling force created by albumin, which favors fluid movement from the ICF into the ECF
35
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
36
hypotonic solution
- more water than blood
- causes shift from ECF to ICF
- 0.45% NaCl
- given for dehydration, for keeping veins open
37
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
38
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
39
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
40
normal Na levels
135-145
41
normal K+ levels
3.5-5.2
42
normal Ca levels
8.7-10
43
normal PO4 levels
2.5-4.5
44
normal Mg++ levels
1.5-2.5
45
s/s hypovolemic hyponatremia
- thirst
- hypotension
- tachycardia
- neurological deficits may develop
46
s/s hypervolemic hyponatremia
- headache
- lethargy
- confusion
- muscle cramps
47
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
48
s/s hyperkalemia
- numbness
- muscle cramps all over
- diarrhea
- ECG changes
- can lead to cardiac arrest
49
s/s hypocalcemia
- neuromuscular excitability
- paresthesia
- hypotension
- cardiac arrhythmias
- chronic: bone pain and fragility
50
s/s hypercalcemia
- decreased neuromuscular excitability
- weakness
- renal calculi
- cardiac arrhythmias
51
s/s hypophosphatemia
- tremors
- muscle weakness
- hyporeflexia
52
s/s hyperphosphatemia
- same as hypocalcemia
- neuromuscular excitability
- paresthesia
- hypotension
- cardiac arrhythmias
53
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
54
s/s hypermagnesemia
- too much neuromuscular relaxation
- muscular flaccidity
- cardiac problems
55
characteristics of arteries
- carry oxygenated blood AWAY from the heart
- pump blood themselves
- high pressure system
- responsible for PULSES
56
arteriosclerosis
hardening/narrowing of the arteries
57
atherosclerosis
plaque buildup in arteries
58
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
59
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
60
what is the primary sign of PAD
intermittent claudication
61
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
61
What is Virchow's triad
- venous stasis
- vascular damage
- hypercoagulability
62
chronic venous insufficiency
- results from damage to deep veins in legs/ incompetent valves which causes impaired venous return
- edema d/t pooling blood
63
clinical presentation CVI
- thin, shiny skin
- dusky discoloration
- edema
- poor healing
- reduced/absent hair distribution
- stasis dermatitis
64
How do we treat CVI
- elevate legs
- wear compression stockings all the time
- SCDs
- anticoagulant or antiplatelet meds
- venoablation
65
normal platelet values
150,000-400,000
66
thrombocytopenia
- low platelet count
- less than 100,000
67
thrombocytosis
- high platelet count
- greater than 750,000
68
what is pt at risk for with platelet count too low
risk for bleeding
69
what is pt at risk for with platelet count too high
risk for clotting
70
extrinsic pathway
- activated when there is injury to the blood vessel from the outside in
- Factor 7 and tissue factor only
71
what lab is extrinsic pathway measured with
PT/INR
72
intrinsic pathway
- activated when there is injury to the blood vessel from inside out
73
what lab is intrinsic pathway measured with
- PTT (Play Table Tennis inside)
- the higher to PTT the higher the risk for bleeding
74
aspirin
- most common antiplatelet drug
- acts on platelets for the life of the platelet
75
warfarin
- better for venous clots
- inhibits Vitamin K
- interferes with vitamin K dependent clotting factors
- monitor with PT/INR
76
heparin
- better for arterial clots
- slows or stops the coagulation pathway
- monitor with PTT
- inhibits intrinsic pathway
77
What is DIC
- disorder of clot formation and bleeding episodes
- clot formation
- depletion of coagulation
- elevated fibrinolysis leads to bleeding
78
What type of patient does DIC happen in?
- critically ill
- develops secondary to other significant disorders, such as septic shock, massive trauma, burns, transfusion
79
how is DIC diagnosed
- elevated D-dimer
- clotting times
- RBC hemolysis
80
how is DIC treated
- control primary disease
- prevent further clotting
- transfuse with FFP (fresh frozen plasma)
81
what is pyelonephritis
- infection of renal pelvis
- ascending UTI
- stasis of urine plays a role
82
what is pyelonephritis caused by
- obstruction somewhere in the renal system
- urine backs up into the kidneys
83
s/s pyelonephritis
- fever
- abdominal or CVA tenderness
- flank pain
- dysuria
- urinary frequency
- microscopic hematuria
- pyuria (WBC in urine)
- + leukocyte esterase test of urine
84
treatment for pyelonephritis
- abx
- analgesics if needed
- fluid intake greater than 3 L/day
- remove urological obstruction, if present
85
what are complications fo pyelonephritis
- chronic pyelonephritis
- which deteriorates into chronic renal insufficiency, which may develop into end stage renal disease
86
what is nephrolithiasis
stones in kidneys
87
risk factors for nephrolithiasis
- genetic susceptibility
- dehydration
- hypercalcemia
- hyperparathyroidism
- gout
- hyperuricemia
- urinary tract infection
- immobility
88
lower urinary tract infection
- most commonly caused by E. coli, originating from bowel
- women at higher risk
- stagnant urine increases infection risk
89
risk factors for lower UTI
- female
- poor hygiene
- taking baths
- BPH
- tight clothing
- dehydration
- diabetes
- sexual intercourse
- pregnancy
- bladder cancer, urinary catheterization (in men)
90
s/s lower UTI
- increased frequency, dysuria, and urgency
- hematuria
- fever (not always present)
91
s/s lower UTI
- increased frequency, dysuria, and urgency
- hematuria
- fever (not always present)
92
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
93
potential complications of UTIs
- urosepsis
- ascending UTI becomes pyelonephritis
94
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
95
leading causes of CRF
- DM
- HTN
96
s/s CRF
- CBC, BUN, and Cr serum levels, urinalysis, albumin levels
- renal imaging studies
97
treatment for CRF
- fluida and electrolyte management, along with BP management
- GFR less than 10-20 mL/min- dialysis, kidney transplant evaluation
98
potential complications of CRF
- encephalopathy
- hyperparathyroidism
- heart failure
- infertility
- thrombocytopenia
- anemia
- electrolyte imbalance
- high BUN
- edema
99
is asthma obstructive or restrictive
obstructive
100
asthma
- hyperreactive airway disease of bronchioles
101
how is asthma diagnosed
PFT during an acute asthma attack
102
treatment for asthma
- stepwise approach
- maintenance medications: daily
- rescue: acute attack
- limit exposure to allergens, know triggers
103
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
104
what do alveoli look like in chronic bronchitis
shrunken alveoli
105
what do alveoli look like in emphysema
- distended, nonrecoiling alveoli
- alveoli lose elasticity
106
how is COPD diagnosed
- COPD assessment test
- PFT's
- CBC, **chest x-ray**, ABG's, ECG
107
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
108
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
109
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
110
primary pneumothorax
just happens , no underlying disease process
111
secondary pneumothorax
lung collapses because of underlying disease process
112
traumatic pneumothorax
penetrating wound to thoracic cage and pleural membrane
113
tension (closed) pneumothorax
closed wound that allows air into the pleural cavity but not out
114
iatrogenic pneumothorax
caused by any medical procedure complications, can often be a parting gift from central line insertion
115
how are primary, secondary, traumatic, and iatrogenic pneumothorax treated
chest tube with suction
116
how is a tension pneumothorax treated
needle insertion to remove air
117
pleural effusion
- abnormal collection of fluid in pleural space
- results of heart failure, severe pulmonary infections
- fluid can be exudate, transudate, purulent, lymph, blood
118
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
119
treatment for pleural effusion
thoracentesis
120
thoracic cage deformity
- anything that structurally makes it hard for lungs to fully inflate
- kyphosis, scoliosis
121
treatment for cage deformity
orthopedic brace
122
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
123
s/s pulmonary fibrosis
- dyspnea
- tachypnea
- crackles
- eventual cyanosis
- CXR results in "ground glass" appearance
124
treatment for pulmonary fibrosis
- try to decrease inflammation/inflammatory response
- may treat with O2
- bronchodilators, corticosteroids
125
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
126
pulmonary embolism
DVT dislodges and travels to lungs
127
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
128
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
129
who is at risk for ARDS
- critically ill patients
- sepsis
- trauma
- massive transfusions
- acute pancreatitis, aspiration
130
what does ARDS require
- intubation, sedation, and mechanical ventilation
- death is common
131
Crohn's disease
- lesions can be anywhere gum to bum
- skip lesions
- cobblestone appearance
- RLQ abdominal pain
132
What is a potential complication of Crohn's disease
toxic megacolon
133
ulcerative colitis
- involves large intestine only
- isolated to the colon and rectum
- ulceration is continuous
- LLQ abdominal pain
- bleeding often occurs
134
GERD
- problem with tone of LES
- regurgitation of stomach acid into esophagus
135
selye's stress response theory
1. alarm
2. resistance
3. exhaustion
136
binge eating
when you just keep eating with no intention of getting rid of food (like inducing vomiting)
137
effects of immobility
- atelectasis
- bone demineralization
- muscle deconditioning
- decubitus ulcers
- depression
- decreased GI motility
- kidney stones
- decreased pulmonary function
- UTI
- venous stasis
138
metabolic alkalosis
- vomiting
- diarrhea
- NG tube suction
- low K+
- low Ca
Tx: treat underlying cause
139
metabolic acidosis
- diabetics and ketoacidosis
- high K+
- high Ca
- Tx: treat underlying cause
140
respiratory alkalosis
- breathing too much CO2 off
- hyperventilation
- high RR
- panic attack
- breath into paper bag
141
respiratory acidosis
- holding onto CO2
- overdose
- low RR
142
normal pH levels
7.35-7.45
143
normal PCO2 levels
35-45
144
normal bicarb levels
22-26
145
fasting blood glucose level for diabetes diagnosis
126 or greater
146
OGTT result for diabetes
200 or greater
147
random glucose level for diabetes diagnosis
200 or greater
148
A1C level for diabetes diagnosis
6.5% or higher
149
what will urinalysis show in diabetes
- ketones
- glucose
150
hyperglycemia cause
- stress
- illness
- eating too much
- dehydration
- lack of exercise
151
s/s hyperglycemia
- polydipsia
- polyuria
- polyphagia
- blurred vision
- electrolyte imbalances
152
treatment for hyperglycemia
- reverse process
- give insulin
153
hypoglycemia cause
- taking too much insulin
- not eating enough carbs
- strenuous exercise
154
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
155
hypoglycemia treatment
- if awake: EAT, foods high in SUGAR
- if asleep: inject DEXTROSE
156
what does the anterior pituitary secrete
- growth hormone
- adrenocorticotropic hormone
- TSH
- FSH
- LH
- prolactin
157
what does the posterior pituitary secrete
- oxytocin
- ADH
158
what does thyroid control
METABOLISM
159
hypothyroidism
- couch potato
- hypercholesterolemia
- gains wt easily
- decreased fertility
- delayed reflexes
- sluggishness
- feeling cold
- constipation
- lethargy
- fatigue
160
hyperthyroidism
- hyperdrive
- anxiety
- tremor
- tachycardia
- feeling warm
- wt loss
- exophthalmos
- atrial fibrillation
- decreased fertility
161
which electrolyte goes with parathyroid
calcium and albumin
162
SIADH
- holding onto water
- excess ADH
- tells kidneys not to diurese
163
s/s SIADH
- same as fluid overload
- hypertension
- swelling
- SOB
164
DI
- insufficient ADH
- kidneys are not told to stop diuresing so you get rid of all your fluid
165
s/s DI
- same as dehydration
- hypotension
- dry mouth
- feeling thirsty
- fatigue
- dark urine
166
diagnostics for SIADH and DI
check adh levels
167
treatment for SIADH and DI
fix underlying cause- pituitary
168
Addison's disease
- adrenal insufficiency
- low sodium
- everything low
169
s/s addisons
- tan skin
- weight loss
- fatigue
- muscle weakness
- light headed
170
Cushing's
- too much cortisol
- immune system depressed
171
s/s cushings
- wt gain
- neck fat/humpback
- moon facies
- easy bruising
- striae
- muscle weakness
172
end organ examples
- bones
- adrenal cortex
- adrenal medulla
- thyroid
- parathyroid
- testes/ovaries
- mammary glands
- uterus
- kidneys
