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patho > exam 2 > Flashcards

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

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2
Q

macule, patch

A

flat, nonpalpable
macule less than 1 cm circumsized border
patch: greater than 1 cm irregular border

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3
Q

macule and patch examples

A

freckles, flat moles, rubella, vitiligo, port wine stains, ecchymosis

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4
Q

papule, plaque

A

elevated, palpable, solid mass
papule: less than 0.5cm
plaque: greater than 0.5cm

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5
Q

papule, plaque examples

A

papule: elevated nevi (mole), warts, lichen planus
plaque: psoriasis, actinic keratosis

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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

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7
Q

nodule, tumor examples

A

nodule: lipoma, squamous cell carcinoma, poorly absorber injection
tumor: larger lipoma, carcinoma

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8
Q

vesicle, bulla

A

circumsribed, elevated, palpable mass with serous fluid
vesicle: less then 0.5cm
Bulla: great than 0.5cm

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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

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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)

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11
Q

wheal examples

A

hives, insect bites

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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

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13
Q

primary disorders of the skin

A

pigmentary disorders
infectious processes
papulosquamos dermatoses
allegic and drug reaction
arthropod infestations

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14
Q

pigmentary skin disorders

A

absence or increase in melanin
-involves melanocytes

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15
Q

pigmentary: vitiligo

A

depigmenting skin disease
etiology unknown
oxidative stress initiated melanocyte destruction
white patches on skin

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16
Q

albinism

A

genetic disorder
complete or partial congenital absense of pigment in skin, hair eyes
ocular problems
nystagmus

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17
Q

melasma

A

darked facial macules
common in brown skin
females more prone
sun exposure makes worse

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18
Q

infectious processes: candidal infection

A

fungal yeast infection caused by C. Albicans
found on skin surface
predisposed to infection: diabetes, immunosuppresion

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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

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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

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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
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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

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23
Q

drug induced skin eruptions

A

localied or generalized eruption
topic drugs responsalbe for localized
systemic drugs cause generalized

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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

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25
Q

erythema multiforme (minor)

A

self limiting
ring like erythematous macules and blisters (red)
central portion is opaque white, yellow/grey

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26
Q

erythema multiforme (major)

A

stevens johnson syndrome
-systemc ulceration of all mucous membranes and skin
-hypersensitivity reaction to drugs (sulfonamides, anticonvulsant, NSAIDS)

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27
Q

toxic epidermal necrolysis (TEN)

A

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

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28
Q

papulosquamous dermatoses psoriasis

A

etiology: gentic, unknown (possible association with arthiritis)
assessment: chronic thickening of epidermis and overlying silver white scales covering red, thickened plaques

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29
Q

antropod infestations: scabies

A
  • 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
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30
Q

pressure injury

A

ischemic lesions of skin and underlying structures
caused by unrelieved pressure that hurts blood flow and lymph
decubitus ulcers

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31
Q

pressure injury- mecahanism of development

A

comorbidities: diabetes
-oxygen deprivation and accumation of metabolic end products

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32
Q

nutrients necessary for wound healing

A

proteins (albumin levels), carbs (energy), vitamic C, zinc, fats

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33
Q

nevi (mole)

A

-most common benign skin tumors
-present as papules and nodules
- atypical or dysplastic: high suspectibility to cancerous change
-need clinical examination

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34
Q

premalignant lesions with nevis

A

1) high nevus count
2) large nevi
(changing in color, size, shape)

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35
Q

malignant melanoma

A

-malignant tumor or melanocytes
-metastaic form of cancer
-mottled: shades of red, blue, white

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36
Q

ABCDE with melanoma

A

A: assymetry
B: border
C: color
D: diameter
E: evolving

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37
Q

basal cell carinoma

A

-neoplasm that develops from basal keratinocytes of epidermis
-non metastisizing
assessment: pinking transluscent papule (pearly) and central depression

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38
Q

squamous cell carcinoma

A

tumor of outer epidermis
-increase UVR reexposure
assessment: red scaling, keratotic, slightly elevated, irregular border, shallow chronic ulcer!

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39
Q

pigmented birth marks

A

mongolian spots, buttocks/sacra areas

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40
Q

port wine stains

A

pink or red patches
persistant throughout life
lesions on face- trigeminal nerve branches

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41
Q

hemangiomas

A

small, red lesion that appear shortly after birth
-benign vascular tumors
-proliferation followed by sow growth- reverser and shrunk by 4yo

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42
Q

hemostasis

A

the stoppage of blood flow

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43
Q

normal hemostasis

A

blood vessel is sealed preventing blood loss and hemmorhage

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44
Q

abnormal hemostasis

A

innapropriate clotting (thrombosis) or insufficient

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45
Q

stage one hemostasis: vascular spasm

A

within 30 min a vascular spasm occurs there is vasoconstriction
-thromboxane A2 is a vasoconstricter released by platelets

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46
Q

stage two hemostasis: formation of platelet plug

A

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

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47
Q

normal platelet count

A

150,000-450,000

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48
Q

clotting factors

A

factors 2, prothrombin, protein c
all synthesized in liver using vitamic K

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49
Q

coagulation process

A

results from intrinsic pathway (slow process- 1-6 min) and extrinsic pathway (15 seconds)

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50
Q

clot retraction

A

occurs 20-60 min after clot formed
clot joins edges of broken blood vessel
requires large number of plateltes

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51
Q

clot dissolution

A

fibrinolysis- blood clot dissolved
plasmin digest fibrin strands of clot
naturally occuring plasminogen activators: tissue-type plasminogen activator

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52
Q

hypercoagulability

A

exaggerated form of hemostasis
predisposed to thrombosis and blood vessel occlusion

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53
Q

two forms of hypercoagulable states

A

1) conditions that increase platelet function
2) conditions that cause accelerated action of the coagulation system

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54
Q

primary thrombocytosis

A

too many platelets
-myeloproliferative (bone marrow) disorder
thrombocytosis: platelet count above a mil

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55
Q

secondary thrombosis

A

disease state that stimulates thrombopoientin production
-damange from surgery, infection, absent spleen

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56
Q

signs ansd symptoms of clotting/thrombosis

A

stroke, tia, shortness of breath, chest pai, hypoxia, no pulse in extremeities, redness/swelling

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57
Q

bleeding disorders

A

impairment of blood coagulation
results from defect in any factors that contribute to hemostasis

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58
Q

thrombocytopenia

A

reduction in platelet numbers less than 150,000

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59
Q

bleeding from platelet disorders

A

results from: decrease platelet production, increased destruction, impaired function
petechiae (pinpoint hemorrhages) or purpura

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60
Q

decreased platelet production

A

aplastic anemia: loss of bone marrow function
normal production but excessive pooling in spleen

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61
Q

reduced platelet survival

A

antiplatelet antibodies (immune destruction)
prosthetic heart valves, DIC

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62
Q

drug induced thrombocytopenia

A

aspirin, atorvastatin, antibiotics, rapid fall in platelet count

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63
Q

heparin induced thrombocytopenia

A

-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

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64
Q

impaired platelet function

A

von willebrand disease
drugs
disease
surgery
uremia
interference with platelet production
warfarin
decrease vitamin K levels: antibiotics

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65
Q

von willebrand disease

A

hereditary bleeding disorder
spontaneuos bleeding
can be life threatening

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66
Q

hemophilia A

A

X linked recessive disorder-primarily males
genetic mutation
mild to moderate forms no bleeding unless procedure

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67
Q

vascular bleeding disorders

A

because of weak or damaged vessels
easy bruising
cushing disease

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68
Q

DIC

A

-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

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69
Q

DIC pathogenesis

A

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

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70
Q

whole blood transfusion

A

everything.. for high volumes of blood loss

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71
Q

PRBC transfusion therapy

A

RBC’s with little plasma for anemia

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72
Q

platelet tranfusion therpay

A

bleeding/prevent bleeding

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73
Q

cryoprecipitate transfusion therapy

A

post surgical, fibrinogen, von willebrand disease, hemophilia

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74
Q

plasma transfusion therapy

A

most common, all coagulation factors, bleeding

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75
Q

anemia

A

abnormally low number of circulating RBCs or hemoglobin
results in diminished oxygen carrying capacity

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76
Q

4 causes of anemia

A

excessive loss of RBC’s from bleeding
-destruction of RBCs
-defective RBC production
-inadequate RBC production due to bone marrow failure

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77
Q

clinical manifestations of anemia

A

-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

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78
Q

MCV

A

mean corpuscular volume
reflects size of RBCs

79
Q

microcytic

A

smaller than normal

80
Q

marcocytic

A

RBC larger than normal

81
Q

normocytic

A

normal RBC size

82
Q

MCHC

A

mean corpuscular hemoglobin concentration
average amount of Hgb in the volume of RBC’s
reflects the color

83
Q

normochomic

A

normal RBC color

84
Q

hypochromic

A

pale RBC color

85
Q

acute blood loss anemia (excessive loss)

A

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
Q

chronic blood loss

A

can lead to iron deficiency anemia
asymptomatic until hemoglobin less than 8
- GI bleeding, mestruation
RBCS have too little hemoglobin
-small pale

87
Q

hemolytic anemia (destruction)

A

-premature destruction of RBCS
-retention of iron
-increase in erythropoeisis(production)
-shortened lifespan- intrinsic and extrensic
-normocytic, normochromic

88
Q

sickle cell disease

A

-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
Q

clinical manifestations of sickle cell

A

-cold weather, stress, infection, diseases that cause hypoxia, pain, jaundice, sluggish blood flow, acute chest syndrome, stroke

90
Q

iron deficiency anemia

A

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
Q

iron deficiency manifestations

A

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
Q

megaloblastic anemia

A

-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
Q

Vitamin B12 deficiency

A

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
Q

B12 deficiency patho

A

Vitamin B12 bounds to intrinisic factor (IF- protein secreted by gastric parietal cells)
-RBCs abnormally large

95
Q

pernicious anemia B12

A

failure to produce IF
-immunologically mediated, possibly autoimmune
other causes; gastrectomy, malabsorption syndromes

96
Q

clinical manifestations of B12 deficiency

A

-jaundice
-neurological changes: parestesias (numbness, tingling) of feet and fingers, loss of vibration, dementia
-macrocytic, normochromic!!

97
Q

Folic acid deficiency B12

A

required for DNA synthesis and RBC maturation
-same as B12 deficiency but NO nuerological

98
Q

Folic acid deficiency etiology

A

dietary deficiency
alcohol supresses folate absorption
celiac disease
macrocytic, normochromic

99
Q

aplastic anemia

A

disorder of bone marrow stem cells that results in reduction of all three hemopoetic cell lines pancotopenia (RBC, RBC, platelets)

100
Q

aplastic anemia etiology

A

high does of radiation, chemotherapy, drugs, autoimmune

101
Q

aplastic anemia manifestations

A

petechia, ecchymoses, bleeding from mouthor nose

102
Q

chronic disease anemia

A

chronic infection, inflammation, cancer
-anemia of renal failure because kidneys are primary site for erythropoietin
-anemia of critical illness (ICU)

103
Q

polycythemia

A

abnormally high RBC mass
etiology: dehydration
increased blood volume- interfering with cardiac output

104
Q

polycythemia manifestations

A

HTN, headache, dizziness, decrease cerebral blood flow, venous stasis, thromboembolism

105
Q

Geriatric considerations for anemia

A

HCT levels are lower after 60
chronic illness
anemia is never normal
nutrition

106
Q

myeloid/bone marrow tissue

A

where WBCS are formed

107
Q

lymph nodes,thymus, spleen

A

where WBCs circulate, mature, and function

108
Q

non neoplastic disorders of WBC
neutropenia

A

less than 1000

109
Q

leukopenia

A

decrease in absolute number of leukocytes in the blood
5000-10000 cells/mm of blood

110
Q

angranulocytosis

A

virtual absense of neutrohpils

111
Q

neutropenia etiology

A

decreased neutrophil production, accelerated utilization or destruction or a shift from blood to tissue compartments
-drug related
-autoimmune
infection
hematologic malignancies

112
Q

hematologic cancers

A

types of cancers that affect blood, bone marrow, and lymph nodes
-either located in blood (leukemia) or lymph nodes (lymphoma)

113
Q

pathopysiology of hematologic disorders

A

-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
Q

non hodgkins lymphoma

A

diverse group of B, T, and NK cell orgins
-arise in the peripheral lymphoid tissue
-chromosomal, EBV

115
Q

NHL manifestations

A

-slow growing or aggresive
-painless swelling of lymphnodes
-aggressive fever, night sweats, weight loss
usually originates are extra nodal sites and moves

116
Q

hodgkins lymphoma

A

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
Q

hodgkins lymphona manifestations

A

painless swelled lymph nodes- first one that swell is above diaphragm
-mediastinal masses
-chest discomfort
-fever, chills, sweats
-fatiguem anemia

118
Q

leukemias

A

-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
Q

lymphocytic leukemia

A

-immature lymphocytes
-originates in bone marrow then infitrates spleen, lymphnodes, CNS
-ALL and CLL

120
Q

myelogenous leukemia

A

myeloid stem cells in bone marrow
-interferes with maturation of all blood cells
-AML and CML

121
Q

etiology of leukemias

A
  • unknown
    -radiation
    -exposure to toxins
    -second cancer
    -genetics
122
Q

ALL acute lymphocytic leukemia

A

involved lymphoblasts
-sudden onset
-children most prone

123
Q

AML acute myelogenous leukemia

A

-myeloid cells in bone marrow
-blast cells- immature cells that supress remaining cells leading to anemia, neutropenia
-older adults

124
Q

ALL and AML manifestations

A

-abrupt onset
-fever
-fatigue
-weight loss
CNS
Leukostasis
hyperuricemia

125
Q

leukostasis

A

circulating blast count is elevated-leukastic emboli

126
Q

hyperuricemia

A

secondary to leukemic cell death from chemotherapy

127
Q

CLL chronic lymphocytic leukemia

A

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
Q

CML chronic myelogenous leukemia

A

philadelphia chromosome present
-terminal blast crisis: represents evolution to acute leukemia very high blast coutns
-WBC over 150000

129
Q

CLL CML manifestations

A

-enlarged spleen
-anemia
-abdominal fullness

130
Q

plasma cell dyscrasia: multiple myeloma

A

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
Q

renal calculi

A

kidney stones
-polycrystalline aggregates composed of material that the kidneys normall excreted in urine
-most common cause of urinary tract obstruction

132
Q

renal calculi etiology

A

-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
Q

types of kidney stones

A

calcium stones (most common), infection stones (struvite), uric acid, cystine stones

134
Q

renal calculi manifestations

A

-renal colic (sharp pain)
-acute to excruciating pain in abdomen of affected side
-radiation to bladder, perineum, scrotum
-cool,clammy

135
Q

UTI

A

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
Q

UTI etiology

A

-urethra enty vs blood stream entry
-E-COLI MOST COMMON
obstruction, reflux, catheter induced, diabetes

137
Q

UTI manifestations

A

frequent urination, low abdominal pain. dysuria, foul smelling, cloudy urine
-fever/infecition usually absent

138
Q

pyelonephritis (tubulointerstitial disease)

A

-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
Q

glomerular disease

A

inflammatory process involving glomerular structures of kidney
-second leading cause of renal failure after diabetes and hypertension

140
Q

glomerular disease- nephrotic syndrome

A

etiology: diabetes and lupus
patho: produces increase in glomerular permeability, low albumin, generalized edema
manifestations: dyspnea. low albumin relating to drugs

141
Q

low albumin relating to drugs

A

some drugs bind to albumin, if there is no albumin to bind to the drugs leak around and cause toxicity

142
Q

acute kidney injury

A

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
Q

common AKI indication: Azotemia

A

accumulation of nitrogenous waste and decreased glomerular filtration rate
-measure by: BUN, GFR (most sensituve), and Creatinine

144
Q

renal physiology

A

-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
Q

test of renal function: serum creatinine

A

-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
Q

Blood urea nitrogen (BUN)

A

-urea is end product of protein metabolism and regulated by kidneys
influenced by: protein intake, GI bleeding, hyrdration status

147
Q

prerenal dysfunction patho

A

marked decrease in renal blood flow

148
Q

prerenal dysfunction etiology

A

-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
Q

prerenal dysfunction manifestations

A

sharp decrease in urine output (oliguria)
elevated BUN
decreased GFR
increased creatinine

150
Q

example prerenal

A

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
Q

intrarenal AKI patho

A

cause damage to the parenchyma (inside tissues) of the kidney

152
Q

intrarenal etiology

A

ischemia and prerenal
toxic insult to kidney
intrabular obstruction
acute pyelonephritis
acute glomerulonephritis
acute ATN
nephrotoxic drugs

153
Q

ATN acute tubular necrosis

A

destruction of tubular epitheiel cells

154
Q

nephrotoxic drugs intrarenal

A

amonoglycoside antibiotics (vancomycin, getamicin)
radiocontrast agents (IV dyes)
cisplatin (chemo agent)
myoglobin r/t muscle truama (dirty brown urine coca cola color)

155
Q

intrarenal example

A

-things in health history that are nephro toxic
-nephro toxic meds? diabetes meds? BP meds?

156
Q

postrenal acute kidney injury patho

A

obstruction of urine outflow from kidney

157
Q

postrenal etiology

A

-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
Q

phase one of AKI

A

onset phase
-hours to days
-time from precipitatiing event to tubular injury

159
Q

phase 2 AKI

A

oliguric phase
-8-14 days
-decrease GFR
-increase potassium
-increase creatinine
-hypertension
-uremia-seizures, death
-fluid retention

160
Q

phase 3 AKI

A

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
Q

phase 4 AKI

A

recovery phase
-tubular swelling resolves
-renal function improves
-normal F&E
-normal labs
-can take a while

162
Q

chronic kidney disease

A

kidney damage of GFR less than 60mL/min for 3 months or longer

163
Q

chronic kidney disease etiology

A

hypertension and diabetes– always want to control these to prevent chronic KD

164
Q

chronic kidney disease patho

A

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
Q

kidney failure

A

GFR- less than 15ml/min
-start renal replacement therapy dialysis or transplant

166
Q

GFR indicator/measurement

A

considered best measure for kidney function

167
Q

albuminuria

A

-early marker for kidney disease because protein leaks out of kidney into urine

168
Q

manifestatios of chronic kidney disease

A

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
Q

most important manifestations

A

-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
Q

intracellular fluid 2/3rd

A

extracellular fluid 1/3

171
Q

diffusion

A

movement of particles along a concentration gradient

172
Q

osmosis

A

movement of water across a semipermeable membrane

173
Q

urine specific gravity

A

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
Q

osmolarity

A

-measurable
-number of osmoles of solute per liter of solution
-RAAS

175
Q

tonicity

A

the effect that the osmotic pressure within a solution exerts on cell size because of water across the cell membrane

176
Q

isotonic- fluid solution

A

same tonicity as blood
.9% normal saline
-cells stay same size
-given to replace normal fluid

177
Q

hypotonic fluid solution

A

less tonicity than blood
-.45% normal saline
-water moves to cells and cells swell
-dont give to someone who is already swelling

178
Q

hypertonic fluid solution

A

greater tonicity than blood
-3% normal saline
-water pulled out from cells and cells shrink

179
Q

Edema

A

palpable swellnig produced by expansion of the interstitial fluid volume ( 10-30ml of fluid)

180
Q

edema patho

A

-increase capillary permeability
inflammation, allergic reaction, tissue injury/burns

181
Q

albumin

A

smallest plasma proteins
-low albumin- edema

182
Q

sodium and water balance: low effective circulating volume

A

activates feedback mechanisms that produce an increase in renal sodium and water retention

183
Q

sodium and water balance: high effective circulating volume

A

triggers feedback mechanisms that decrease the sodium and water retention

184
Q

baroreceptors

A

sense volume status and alter them to maintain sodium and water balance

185
Q

RAAS!!!

A
186
Q

thirst

A

regulator of water intake

187
Q

isotonic fluid volume deficitit

A

decrease in ECF/circulating blood volume
proportionate losses in sodium and water

188
Q

isotonic FVD etiology

A

inadequate fluid intake(unconsious, withholding, impaired thirst sensor
-excessive GI loss
-skin loss (burn, fever)
third space loss (edema interstitial fluid)

189
Q

isotonic FVD manifestations

A

weight loss, decrease urine output(body is conserving urine), increase osmolality, thirst, increase BUN/creatinine, hypotension, thready pulse, sunken eyes

190
Q

isotonic fluid volume excess

A

expansion of the ECF compartment with increased interstitial and vascular volume
compensatory (good) vs pathologic (bad)

191
Q

isotonic FVE etiology

A

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
Q

isotonic FVE manifestations

A

weight gain, edema, full bounding pulse, pulmonary edema (crackles, SOB)

193
Q

sodium imbalance

A

normal sodium- 135-145 MEq/L
-common electrolyte disorder
-age-related events

194
Q
A

patho (5 decks)

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