exam 2 Flashcards
1
Q
functions of skin
A
protects from the elements in external environment
-immune regulation
-somatosensory function
-temp regulation
-barrier protection
-vitamin D synthesis
2
Q
macule, patch
A
flat, nonpalpable
macule less than 1 cm circumsized border
patch: greater than 1 cm irregular border
3
Q
macule and patch examples
A
freckles, flat moles, rubella, vitiligo, port wine stains, ecchymosis
4
Q
papule, plaque
A
elevated, palpable, solid mass
papule: less than 0.5cm
plaque: greater than 0.5cm
5
Q
papule, plaque examples
A
papule: elevated nevi (mole), warts, lichen planus
plaque: psoriasis, actinic keratosis
6
Q
nodule, tumor
A
evelated, palpable, solid mass that extends into deeper dermis
nodule: 0.5-2 cm circumscribed
tumor: great than 1-2 cm does not always have sharp border
7
Q
nodule, tumor examples
A
nodule: lipoma, squamous cell carcinoma, poorly absorber injection
tumor: larger lipoma, carcinoma
8
Q
vesicle, bulla
A
circumsribed, elevated, palpable mass with serous fluid
vesicle: less then 0.5cm
Bulla: great than 0.5cm
9
Q
vesicle bulla examples
A
vescicles: herpes simple, varicella, poison ivy, second degree burn blister
Bulla: pemphigus, dermatiss, large burn blisters, poison ivy, bullous impetigo
10
Q
wheal
A
elevated mass with transient borders, irregular, varying size and color
-caused by movement of serous fluid into dermis (not free fluid in cavity)
11
Q
wheal examples
A
hives, insect bites
12
Q
scar
A
skin mark left after healing wound
-replacement by connective tissue of injured tissue
young scars: red and purple
mature scars: white and glistening
13
Q
primary disorders of the skin
A
pigmentary disorders
infectious processes
papulosquamos dermatoses
allegic and drug reaction
arthropod infestations
14
Q
pigmentary skin disorders
A
absence or increase in melanin
-involves melanocytes
15
Q
pigmentary: vitiligo
A
depigmenting skin disease
etiology unknown
oxidative stress initiated melanocyte destruction
white patches on skin
16
Q
albinism
A
genetic disorder
complete or partial congenital absense of pigment in skin, hair eyes
ocular problems
nystagmus
17
Q
melasma
A
darked facial macules
common in brown skin
females more prone
sun exposure makes worse
18
Q
infectious processes: candidal infection
A
fungal yeast infection caused by C. Albicans
found on skin surface
predisposed to infection: diabetes, immunosuppresion
19
Q
bacterial skin infection
A
bacteria are normal flora of the skin
-cellulitis: affects dermis and SUBQ tissues
-S. aureus
-fever, erythema, heat, edema, and pain
20
Q
viral infection of skin
A
rely on live cells of host
risk factors: corticosteriods, antibiotics
herpes simplex (HSV 1), coldsores
herpes (HSV 2) genital
herpes zoster (shingles) vesicular eruption over a dermatomal segment of the skin
21
Q
allergic and hypersensitivity dermatoses
A
- involve inflammatory response to multople exogenous and endogenous agents
characterized by epidermal edema with separation epiderma cells
-drug induced skin eruptions - urticaria
22
Q
Uticaria (allergy/ hypersensitivtiy)
A
pale, raised, itchy papules
-immunologic reaction to antigen in an IGE hypersensitivity response
-histamine release
-etiology: foods, meds, insects
angioedema
swelling of tongue and airway
23
Q
drug induced skin eruptions
A
localied or generalized eruption
topic drugs responsalbe for localized
systemic drugs cause generalized
24
Q
drug induced skin eruptions
A
epidermal skin detachment and formation of bullous lesions
1 erythema multiforme minor
2 steven johnson syndrome
3 toxic epidermal necrolysis
25
erythema multiforme (minor)
self limiting
ring like erythematous macules and blisters (red)
central portion is opaque white, yellow/grey
26
erythema multiforme (major)
stevens johnson syndrome
-systemc ulceration of all mucous membranes and skin
-hypersensitivity reaction to drugs (sulfonamides, anticonvulsant, NSAIDS)
27
toxic epidermal necrolysis (TEN)
most serious drug reaction
prodromal: malaise, low grade fever, sore throat
-wide spread erythema
-large bullae
-loss of epidermis
-mucousal surfaces involved- eyes mouth can lead to blindness
28
papulosquamous dermatoses psoriasis
etiology: gentic, unknown (possible association with arthiritis)
assessment: chronic thickening of epidermis and overlying silver white scales covering red, thickened plaques
29
antropod infestations: scabies
- caused by mites
-spread by skin to skin contact, objects, clothing, bedding
-small papules
-visible wavy or linear burrows ( webbed fingers and toes, folds of skins, nipples, genitalia)
lesions are itchy, excoriated
30
pressure injury
ischemic lesions of skin and underlying structures
caused by unrelieved pressure that hurts blood flow and lymph
decubitus ulcers
31
pressure injury- mecahanism of development
comorbidities: diabetes
-oxygen deprivation and accumation of metabolic end products
32
nutrients necessary for wound healing
proteins (albumin levels), carbs (energy), vitamic C, zinc, fats
33
nevi (mole)
-most common benign skin tumors
-present as papules and nodules
- atypical or dysplastic: high suspectibility to cancerous change
-need clinical examination
34
premalignant lesions with nevis
1) high nevus count
2) large nevi
(changing in color, size, shape)
35
malignant melanoma
-malignant tumor or melanocytes
-metastaic form of cancer
-mottled: shades of red, blue, white
36
ABCDE with melanoma
A: assymetry
B: border
C: color
D: diameter
E: evolving
37
basal cell carinoma
-neoplasm that develops from basal keratinocytes of epidermis
-non metastisizing
assessment: pinking transluscent papule (pearly) and central depression
38
squamous cell carcinoma
tumor of outer epidermis
-increase UVR reexposure
assessment: red scaling, keratotic, slightly elevated, irregular border, shallow chronic ulcer!
39
pigmented birth marks
mongolian spots, buttocks/sacra areas
40
port wine stains
pink or red patches
persistant throughout life
lesions on face- trigeminal nerve branches
41
hemangiomas
small, red lesion that appear shortly after birth
-benign vascular tumors
-proliferation followed by sow growth- reverser and shrunk by 4yo
42
hemostasis
the stoppage of blood flow
43
normal hemostasis
blood vessel is sealed preventing blood loss and hemmorhage
44
abnormal hemostasis
innapropriate clotting (thrombosis) or insufficient
45
stage one hemostasis: vascular spasm
within 30 min a vascular spasm occurs there is vasoconstriction
-thromboxane A2 is a vasoconstricter released by platelets
46
stage two hemostasis: formation of platelet plug
small breaks in vessel wall are sealed by platelet plug instead of a clot
platelet plug formatio involved activation, adhesion, and aggregation of platelets
- glycoprotein binds fibrinogen and links platelets togethers
-requires protein willebrand factor
47
normal platelet count
150,000-450,000
48
clotting factors
factors 2, prothrombin, protein c
all synthesized in liver using vitamic K
49
coagulation process
results from intrinsic pathway (slow process- 1-6 min) and extrinsic pathway (15 seconds)
50
clot retraction
occurs 20-60 min after clot formed
clot joins edges of broken blood vessel
requires large number of plateltes
51
clot dissolution
fibrinolysis- blood clot dissolved
plasmin digest fibrin strands of clot
naturally occuring plasminogen activators: tissue-type plasminogen activator
52
hypercoagulability
exaggerated form of hemostasis
predisposed to thrombosis and blood vessel occlusion
53
two forms of hypercoagulable states
1) conditions that increase platelet function
2) conditions that cause accelerated action of the coagulation system
54
primary thrombocytosis
too many platelets
-myeloproliferative (bone marrow) disorder
thrombocytosis: platelet count above a mil
55
secondary thrombosis
disease state that stimulates thrombopoientin production
-damange from surgery, infection, absent spleen
56
signs ansd symptoms of clotting/thrombosis
stroke, tia, shortness of breath, chest pai, hypoxia, no pulse in extremeities, redness/swelling
57
bleeding disorders
impairment of blood coagulation
results from defect in any factors that contribute to hemostasis
58
thrombocytopenia
reduction in platelet numbers less than 150,000
59
bleeding from platelet disorders
results from: decrease platelet production, increased destruction, impaired function
petechiae (pinpoint hemorrhages) or purpura
60
decreased platelet production
aplastic anemia: loss of bone marrow function
normal production but excessive pooling in spleen
61
reduced platelet survival
antiplatelet antibodies (immune destruction)
prosthetic heart valves, DIC
62
drug induced thrombocytopenia
aspirin, atorvastatin, antibiotics, rapid fall in platelet count
63
heparin induced thrombocytopenia
-immobile people
-immune reaction directed against a complex of heparin and platelet factor 4
bindin of antibody to PF4 produced immunr complrexes that activate the remaining platelets leading to thrombosis
64
impaired platelet function
von willebrand disease
drugs
disease
surgery
uremia
interference with platelet production
warfarin
decrease vitamin K levels: antibiotics
65
von willebrand disease
hereditary bleeding disorder
spontaneuos bleeding
can be life threatening
66
hemophilia A
X linked recessive disorder-primarily males
genetic mutation
mild to moderate forms no bleeding unless procedure
67
vascular bleeding disorders
because of weak or damaged vessels
easy bruising
cushing disease
68
DIC
-something has occured that activated the coagulation system causing little clots all over the body
-widespread coagulation as a compilation of variety of conditions
can cause severe hemmorhage
69
DIC pathogenesis
1) significant illness
2) activation of abnormal fibrinolysis (intitial or later)
3) thrombus formation
4) tissue ischemia
5) end organ damage
6) end organ failure
70
whole blood transfusion
everything.. for high volumes of blood loss
71
PRBC transfusion therapy
RBC's with little plasma for anemia
72
platelet tranfusion therpay
bleeding/prevent bleeding
73
cryoprecipitate transfusion therapy
post surgical, fibrinogen, von willebrand disease, hemophilia
74
plasma transfusion therapy
most common, all coagulation factors, bleeding
75
anemia
abnormally low number of circulating RBCs or hemoglobin
results in diminished oxygen carrying capacity
76
4 causes of anemia
excessive loss of RBC's from bleeding
-destruction of RBCs
-defective RBC production
-inadequate RBC production due to bone marrow failure
77
clinical manifestations of anemia
-mucous membranes, eyes, and skin pale
-oxygen carrying capacity of hemoglobin is reduced
-lab tests
-fatigue
-headache
-pallor of skin, jaundice
-tachycardia, palpitations
-petechia, purpura
78
MCV
mean corpuscular volume
reflects size of RBCs
79
microcytic
smaller than normal
80
marcocytic
RBC larger than normal
81
normocytic
normal RBC size
82
MCHC
mean corpuscular hemoglobin concentration
average amount of Hgb in the volume of RBC's
reflects the color
83
normochomic
normal RBC color
84
hypochromic
pale RBC color
85
acute blood loss anemia (excessive loss)
up to 50% of RBC mass can be lost
can also be related to hemodilution (low hemoglobing and hematrocrit)
RBCs return to normal 3-5 days after intervention
-nomocytic, normochomic!!
86
chronic blood loss
can lead to iron deficiency anemia
asymptomatic until hemoglobin less than 8
- GI bleeding, mestruation
RBCS have too little hemoglobin
-small pale
87
hemolytic anemia (destruction)
-premature destruction of RBCS
-retention of iron
-increase in erythropoeisis(production)
-shortened lifespan- intrinsic and extrensic
-normocytic, normochromic
88
sickle cell disease
-abnormal substitution of an amino acid in the hemoglobin molecules
-inherited disorder in which abnormal hemoglobin (hemoglobin S [hbS]) leads to chronic hemplytic anemia, pain, organ failire
-disproportionally affects people with african heritage
-etiology- point mutation in the B chain of hemoglobin
89
clinical manifestations of sickle cell
-cold weather, stress, infection, diseases that cause hypoxia, pain, jaundice, sluggish blood flow, acute chest syndrome, stroke
90
iron deficiency anemia
etiology: dietary, loss of iron
anemia comes form chronic blood loss-inadequate iron available for recycling
-impoverished populations, vegetarians, gi bleed, menstruation, pregancy
-microcytic, hypochromic
91
iron deficiency manifestations
related to impaired oxygen trasport
fatigute, palpitations, dyspenia
pica: craving clay and ice
spoon shaped fingernails
glossitis- smooth shiny tongue
angular chelitits sores in corners of mouth
92
megaloblastic anemia
-caused by impaired DNA synthesis that results in enlarged red cells
MCHC normal
-developed slowly
-caused by Vitamin B12 deficiency and folic acid deficiencies
93
Vitamin B12 deficiency
essential for DNA synthesis and nuclear maturation- leads to normal RBC maturation and division
-predisposed to myelin breakdown- neurologic symptoms!!
-risk factors: proton pump inhibitores (prylosec), GI disease
-numbness, tingling
94
B12 deficiency patho
Vitamin B12 bounds to intrinisic factor (IF- protein secreted by gastric parietal cells)
-RBCs abnormally large
95
pernicious anemia B12
failure to produce IF
-immunologically mediated, possibly autoimmune
other causes; gastrectomy, malabsorption syndromes
96
clinical manifestations of B12 deficiency
-jaundice
-neurological changes: parestesias (numbness, tingling) of feet and fingers, loss of vibration, dementia
-macrocytic, normochromic!!
97
Folic acid deficiency B12
required for DNA synthesis and RBC maturation
-same as B12 deficiency but NO nuerological
98
Folic acid deficiency etiology
dietary deficiency
alcohol supresses folate absorption
celiac disease
macrocytic, normochromic
99
aplastic anemia
disorder of bone marrow stem cells that results in reduction of all three hemopoetic cell lines pancotopenia (RBC, RBC, platelets)
100
aplastic anemia etiology
high does of radiation, chemotherapy, drugs, autoimmune
101
aplastic anemia manifestations
petechia, ecchymoses, bleeding from mouthor nose
102
chronic disease anemia
chronic infection, inflammation, cancer
-anemia of renal failure because kidneys are primary site for erythropoietin
-anemia of critical illness (ICU)
103
polycythemia
abnormally high RBC mass
etiology: dehydration
increased blood volume- interfering with cardiac output
104
polycythemia manifestations
HTN, headache, dizziness, decrease cerebral blood flow, venous stasis, thromboembolism
105
Geriatric considerations for anemia
HCT levels are lower after 60
chronic illness
anemia is never normal
nutrition
106
myeloid/bone marrow tissue
where WBCS are formed
107
lymph nodes,thymus, spleen
where WBCs circulate, mature, and function
108
non neoplastic disorders of WBC
neutropenia
less than 1000
109
leukopenia
decrease in absolute number of leukocytes in the blood
5000-10000 cells/mm of blood
110
angranulocytosis
virtual absense of neutrohpils
111
neutropenia etiology
decreased neutrophil production, accelerated utilization or destruction or a shift from blood to tissue compartments
-drug related
-autoimmune
infection
hematologic malignancies
112
hematologic cancers
types of cancers that affect blood, bone marrow, and lymph nodes
-either located in blood (leukemia) or lymph nodes (lymphoma)
113
pathopysiology of hematologic disorders
-nonfunctional, cancerous WBC proliferate and overwhelm the bone marrow
-cancerous WBC increase to excess numbers which crowd and suppres development of other cells in bone marrow
-damage turns on oncogenes or turns off tumor supressor genes
114
non hodgkins lymphoma
diverse group of B, T, and NK cell orgins
-arise in the peripheral lymphoid tissue
-chromosomal, EBV
115
NHL manifestations
-slow growing or aggresive
-painless swelling of lymphnodes
-aggressive fever, night sweats, weight loss
usually originates are extra nodal sites and moves
116
hodgkins lymphoma
malignancy of B lymphocytes
- bimodal- early adults or older adults
-arises in single node or chain
etiology: unknown, carcinogen exposure, viruses, immune
-presence of reed steinberg cells in lymphoid tissue
117
hodgkins lymphona manifestations
painless swelled lymph nodes- first one that swell is above diaphragm
-mediastinal masses
-chest discomfort
-fever, chills, sweats
-fatiguem anemia
118
leukemias
-malignant neoplasms of cells orginally derived from single blood cell line derived from hemapoietic stem cells
-leukemia cell spill out into blood
-most common in kids
119
lymphocytic leukemia
-immature lymphocytes
-originates in bone marrow then infitrates spleen, lymphnodes, CNS
-ALL and CLL
120
myelogenous leukemia
myeloid stem cells in bone marrow
-interferes with maturation of all blood cells
-AML and CML
121
etiology of leukemias
- unknown
-radiation
-exposure to toxins
-second cancer
-genetics
122
ALL acute lymphocytic leukemia
involved lymphoblasts
-sudden onset
-children most prone
123
AML acute myelogenous leukemia
-myeloid cells in bone marrow
-blast cells- immature cells that supress remaining cells leading to anemia, neutropenia
-older adults
124
ALL and AML manifestations
-abrupt onset
-fever
-fatigue
-weight loss
CNS
Leukostasis
hyperuricemia
125
leukostasis
circulating blast count is elevated-leukastic emboli
126
hyperuricemia
secondary to leukemic cell death from chemotherapy
127
CLL chronic lymphocytic leukemia
malignancy of B lymphocytes
-most common form
-rapidly fatal
-septic shock
-growth of lymph nodes
WBC over 20000
hypogammaglobulinemia: lack of hemoglobin leads to increase risk of infections
128
CML chronic myelogenous leukemia
philadelphia chromosome present
-terminal blast crisis: represents evolution to acute leukemia very high blast coutns
-WBC over 150000
129
CLL CML manifestations
-enlarged spleen
-anemia
-abdominal fullness
130
plasma cell dyscrasia: multiple myeloma
expansion of immunoglobin producing plasma cell
b cell malignancy of plasma cells
proliferating osteoclasts due to unregulated production of monoclonal antibody (m proteins or bence jones proteins
131
renal calculi
kidney stones
-polycrystalline aggregates composed of material that the kidneys normall excreted in urine
-most common cause of urinary tract obstruction
132
renal calculi etiology
-increase in stone components
-anatomy changes in urinary tract structures
-metabolic and endocrine
-dietary and intestinal absorption
-UTIs
-super saturated urine for stone to grow (can initiate anywhere)
133
types of kidney stones
calcium stones (most common), infection stones (struvite), uric acid, cystine stones
134
renal calculi manifestations
-renal colic (sharp pain)
-acute to excruciating pain in abdomen of affected side
-radiation to bladder, perineum, scrotum
-cool,clammy
135
UTI
infection facilititated by a condition in host that the urinary cannot wash out
-urine flow, change in protective properties of mucin lining, disruption of protective function of normal flora, impaired immune system
-virulence of microorganism helo evade local defenses-bacteria must adhere to epitherlials cells of urinary tract
136
UTI etiology
-urethra enty vs blood stream entry
-E-COLI MOST COMMON
obstruction, reflux, catheter induced, diabetes
137
UTI manifestations
frequent urination, low abdominal pain. dysuria, foul smelling, cloudy urine
-fever/infecition usually absent
138
pyelonephritis (tubulointerstitial disease)
-caused from uti
-acute: upper UTI from gram negative e coli that goes up into kidneys- chills, fever, CVA tenderness, UTI symptoms
-Chronic: progessive, results in kidney scarring, bacterial infection superimposed on obstructive abnormalites or reflux
139
glomerular disease
inflammatory process involving glomerular structures of kidney
-second leading cause of renal failure after diabetes and hypertension
140
glomerular disease- nephrotic syndrome
etiology: diabetes and lupus
patho: produces increase in glomerular permeability, low albumin, generalized edema
manifestations: dyspnea. low albumin relating to drugs
141
low albumin relating to drugs
some drugs bind to albumin, if there is no albumin to bind to the drugs leak around and cause toxicity
142
acute kidney injury
acute insult to kidney that causes rapid decline in function
-build up of nitrogenous waste
-impairs fluid and electrolyte
-reverisible is factors corrected
-mortality rate 20-60%
older adults sepsis, medication, cadiogenic shock
143
common AKI indication: Azotemia
accumulation of nitrogenous waste and decreased glomerular filtration rate
-measure by: BUN, GFR (most sensituve), and Creatinine
144
renal physiology
-regulated PH
-regulated osmolality of ECH and antidieuretic hormone
-regulate BP through RAAS
-regulated RBC production
-concentrated urine
-remove metabolic wastes
-removes and regulated fluids
-activated vitamin D
145
test of renal function: serum creatinine
-best measurement
-creatinine is waste product of muscle metabolism that is complete excreted and can be a measure for kidney filtration
-elevated with kidney dysfunction
-GFR, specific gravity, urine osmolity
146
Blood urea nitrogen (BUN)
-urea is end product of protein metabolism and regulated by kidneys
influenced by: protein intake, GI bleeding, hyrdration status
147
prerenal dysfunction patho
marked decrease in renal blood flow
148
prerenal dysfunction etiology
-depletion of vascular volume(decreases renal BF)
-hemmorage
-dehydration (vomiting, bleeding what did pt come in with)
-loss of ECF volume
-decreased vascular filling
shock states (septic, anaphlx)
-decreased perfusion (heart problems)
-vasoactive mediators (drugs, diagnostic agents) vasoconstriction
149
prerenal dysfunction manifestations
sharp decrease in urine output (oliguria)
elevated BUN
decreased GFR
increased creatinine
150
example prerenal
70 y/o with GI bleed, diabetes, hypertension with BP 85/50, HR 140 lost a lot of blood during surgery
decreased urine output and increase creatinine
151
intrarenal AKI patho
cause damage to the parenchyma (inside tissues) of the kidney
152
intrarenal etiology
ischemia and prerenal
toxic insult to kidney
intrabular obstruction
acute pyelonephritis
acute glomerulonephritis
acute ATN
nephrotoxic drugs
153
ATN acute tubular necrosis
destruction of tubular epitheiel cells
154
nephrotoxic drugs intrarenal
amonoglycoside antibiotics (vancomycin, getamicin)
radiocontrast agents (IV dyes)
cisplatin (chemo agent)
myoglobin r/t muscle truama (dirty brown urine coca cola color)
155
intrarenal example
-things in health history that are nephro toxic
-nephro toxic meds? diabetes meds? BP meds?
156
postrenal acute kidney injury patho
obstruction of urine outflow from kidney
157
postrenal etiology
-bilateral obstruction in ureter (stricture, calculi)
-bladder outlet obstruction (tumors)
-urethra (prostatic hyperplasia)
-retrograde pressure increases and damage to nephrons
-back flow of urine
158
phase one of AKI
onset phase
-hours to days
-time from precipitatiing event to tubular injury
159
phase 2 AKI
oliguric phase
-8-14 days
-decrease GFR
-increase potassium
-increase creatinine
-hypertension
-uremia-seizures, death
-fluid retention
160
phase 3 AKI
diuretic phase
-urine output increases (does not mean going back to normal)
-Fluid and electrolyte abnormalities
-tubule damage
-diuresis before renal function normal
-increase potassium, BUN, creatinine
161
phase 4 AKI
recovery phase
-tubular swelling resolves
-renal function improves
-normal F&E
-normal labs
-can take a while
162
chronic kidney disease
kidney damage of GFR less than 60mL/min for 3 months or longer
163
chronic kidney disease etiology
hypertension and diabetes-- always want to control these to prevent chronic KD
164
chronic kidney disease patho
decline in kidney function because of permant loss of nephrons
-deterioration of glomerular filtration, tubular resporption, and endocrine functions
- kidneys not doing anything they supposed to
165
kidney failure
GFR- less than 15ml/min
-start renal replacement therapy dialysis or transplant
166
GFR indicator/measurement
considered best measure for kidney function
167
albuminuria
-early marker for kidney disease because protein leaks out of kidney into urine
168
manifestatios of chronic kidney disease
accumulation of nitrogenous waste
-high BUN
-electrolyte imbalance
-acid base imbalance
-chronic anemia
-coagulation disorders
-mineral/skeletal issues
-hypertension/CV issues
-neuro issues: encephaopathy (change in mental status)
-skin integrety
-immune system
-GI issues
169
most important manifestations
-accumulation of nitrogenous waste: urea-high BUN
uremia: altered F&E, acid base balance, encephalopathy, itching
- F&E/ acid base imbalance: volume regulation, polyuria, hyperkalemia,metabolic acidosis
170
intracellular fluid 2/3rd
extracellular fluid 1/3
171
diffusion
movement of particles along a concentration gradient
172
osmosis
movement of water across a semipermeable membrane
173
urine specific gravity
compares weight or urine to water- reflects kidneys ability to produce a concentrated or diluted urine based on serum osmolality and the need for water conservation and excretion
174
osmolarity
-measurable
-number of osmoles of solute per liter of solution
-RAAS
175
tonicity
the effect that the osmotic pressure within a solution exerts on cell size because of water across the cell membrane
176
isotonic- fluid solution
same tonicity as blood
.9% normal saline
-cells stay same size
-given to replace normal fluid
177
hypotonic fluid solution
less tonicity than blood
-.45% normal saline
-water moves to cells and cells swell
-dont give to someone who is already swelling
178
hypertonic fluid solution
greater tonicity than blood
-3% normal saline
-water pulled out from cells and cells shrink
179
Edema
palpable swellnig produced by expansion of the interstitial fluid volume ( 10-30ml of fluid)
180
edema patho
-increase capillary permeability
inflammation, allergic reaction, tissue injury/burns
181
albumin
smallest plasma proteins
-low albumin- edema
182
sodium and water balance: low effective circulating volume
activates feedback mechanisms that produce an increase in renal sodium and water retention
183
sodium and water balance: high effective circulating volume
triggers feedback mechanisms that decrease the sodium and water retention
184
baroreceptors
sense volume status and alter them to maintain sodium and water balance
185
RAAS!!!
186
thirst
regulator of water intake
187
isotonic fluid volume deficitit
decrease in ECF/circulating blood volume
proportionate losses in sodium and water
188
isotonic FVD etiology
inadequate fluid intake(unconsious, withholding, impaired thirst sensor
-excessive GI loss
-skin loss (burn, fever)
third space loss (edema interstitial fluid)
189
isotonic FVD manifestations
weight loss, decrease urine output(body is conserving urine), increase osmolality, thirst, increase BUN/creatinine, hypotension, thready pulse, sunken eyes
190
isotonic fluid volume excess
expansion of the ECF compartment with increased interstitial and vascular volume
compensatory (good) vs pathologic (bad)
191
isotonic FVE etiology
inadequate sodium and water elimination due to heart failure, renal failure, cushing disease, liver failure
-excessive sodium intake (causes pt to retain fluid) (think thanksgiving)
-admin of fluid at high rate
192
isotonic FVE manifestations
weight gain, edema, full bounding pulse, pulmonary edema (crackles, SOB)
193
sodium imbalance
normal sodium- 135-145 MEq/L
-common electrolyte disorder
-age-related events
194
