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Pharm/Patho > Sem2Midterm > Flashcards

Sem2Midterm Flashcards

1
Q

What are the three classifications of systems for anti-bitoics?

A

1-By Susceptible organism (broad or narrow spectrum)
2- BY bactericidal vs. bacteriostatic
3- By mechanisms of action

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2
Q

What does it mean when a drug is bacteriocidal?

A

It is lethal to the bacteria at clinically achievable concentrations and the bacteria dies

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3
Q

What does it mean when a drug is bacteriostatic?

A

This means that the bacterial growth will SLOW, but not die. The host will eventually eliminate the organism through phagocytes

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4
Q

What are the 4 antimicrobial mechanisms of action?

A

Cell wall synthesis inhibitor
Protein synthesis inhibitor
DNA synthesis inhibitor
Metabolism Inhibitor (folate antagonist)

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5
Q

Why are penicillins and Cephalosporins similar?

A

The both contain the beta-lactam structure

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6
Q

Amoxicillin

A 
Oral- Broad spectrum- 250mg-500 q8h
Gram neg and pos organisms 
Eliminated through renal system
AE: hypersensitivity, diarrhea *take with food*
Caution with oral contraceptives
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7
Q

What is beta-lactamase?

A

An enzyme that some bacteria produce that breaks down the beta lactam ring in penicillins and cephalosporins
-can be specific

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8
Q

What is a beta- lactamase inhibitor ?

A

chemical compound that is to be taken WITH antibiotic so that the break-down of beta lactam is prevented.

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9
Q

What is Augmentin made up of?

A

Clauvuanic Acid and amoxicillin

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10
Q

What is Unasyn made up of?

A

Ampicillin and sulbactam

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11
Q

What is Zosyn made up of?

A

piperacillin and tazobactam

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12
Q

Amoxicillin and Clavulanic Acid

A

amniopenicillin and a beta- lactamase inhibitor 250-1000 q8-12hrs
gram neg and pos
Extends to organisms that so produce beta lactamase
ex) H. INfluenza
AE: Hypersensitivity, diarrhea, may take with food
* Cell Wall Synthesis Inhibitor*

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13
Q

Piperacillin-Tazobactam

A

Extended Spectrum- 2.25-4.5 g IV q6h (none orally)
Gram pos and neg
AE: HYpersensitivity, diarrhea
Cell Wall Synthesis Inhibitor

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14
Q

How are cephalosporins grouped?

A

Into generations based on
1- Effectiveness against different organisms
2- Characteristics
3-Develpment

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15
Q

How common is cross sensitivity with PCN and Cephalosporins?

A

5%

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16
Q

What is an example of 1st generation cephalosporin?

A

Cephalexin- Keflex

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17
Q

What is an example of a 3rd generation cephalosporin?

A

Cefriaxone - Rocephin

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18
Q

What are 5 examples of Cell wall synthesis inhibitors?

A 
Amoxicillin
Amoxicillin + Clavulanic acid
Piperacillin + Tazobactam
Cephalexin
Cefriaxone
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19
Q

Cephalexin

A

Oral 250-1000mg Q6-8hr
Gram pos (skin flora)
1st gen
AE: nausea, vomiting, diarrhea - take with food

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20
Q

Ceftiaxone

A 
IV or IM 250-2g IV/IM Q12-24 hrs
3rd Gen
** BEST FOR step. pneum. and Gonorr
Gram pos and neg
AE: Hypersensitivity, may increase bleeding
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21
Q

What are the contraindications for cefriaxone?

A

Avoid in neonates- may displace bilirubin from albumin binding sites

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22
Q

What are 4 ways a protein synthesis inhibitor could work?

A

1-inhibit formation of peptide bond
2- prevents tRNA and mRNA from attatching with ribosome complex
3- Prevent movement of ribosome movement
4- Causes code mRNA to read code wrong

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23
Q

Doxycycline

A

IV/PO 100 mg q12hr (tetracyline class)
gram pos and neg –Bacteriostatic- broad
Protein synthesis inhibitor
*BEST FOR chlamydia and tick borne illness
AE: phototoxicity, tooth discoloration, C.Diff

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24
Q

What are some considerations to think about with doxycyline?

A

Don’t take with milk, antacids or oral contraceptives

Don’t take if pregnant or under 8

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25
Q

Azithromycin

A

IV/PO- 250mg-500 daily (macrolides)
can cover atypical- mycoplasma, legionella and chlamydia
AE: nausea, vomiting, abd pain, some QT prolonged on EKG
bacteriostatic (cidal in high doses)- broad

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26
Q

How does tetracycline/ doxycycline work on protein synthesis inhibition?

A

interferes with attachment of tRNA to mRNA ribosome complex

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27
Q

How does azythromycin work as protein synthesis inhibitor?

A

reversibly binds to ribosomal subunit

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28
Q

Metronidazole

A

IV/PO 250-750 mg q8-12 hr
bacteriocidal- fiarly narrow- protozoa *systemic amebiasus, trichomonasis, giardiasis
AE: nausea, headache, metallic taste, hypersensitivity
drug interaction with ethanol-tachy, dysnea, vomit, facial flushing

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29
Q

What is metronidazole MOA?

A

inhibits nucleic acid synthesis=cell death

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30
Q

What are the two categories of antifungal drugs?

A

SubQ/ systemic

superficial

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31
Q

Fluconazole

A

IV/PO 200-800mg q24hr member of azole family
fungistatic- damage of membrane
BEST FOR candida infections
AE: nausea, headache, rash, adb pain, (rare=hepatic necrosis)

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32
Q

Anticoagulant Medications are used to…?

A

prevent clots from forming and extension
prevent and treat VTE&PE
Stroke prevention in atrial fib
HIgh risk for VTE

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33
Q

Who are at high risk for VTE?

A

hospitalized patients who are less mobile
Post-op orthopedic surgery
artificial heart vavles
heart failure

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34
Q

What is an example of an unfractionated heparin & low-molecular weight heparin?

A

Heparin and Enoxaparin

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35
Q

What is an exmaple of a vitamin K antagonist?

A

Warfarin- inhibits synthesis of vit k- dependent clotting factors

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36
Q

What is an example of a direct thrombin inhibitor?

A

Dabigatran

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37
Q

What is an exmaple of factor Xa inhibitor?

A

Rivaroxaban

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38
Q

What 3 things does thrombin do?

A

1 catalyze conversion- fibrinogen–>fibrin
2 catalyze conversion - Factor V –> active Va (inhances activity of Xa)
3 catalyze conversion- VIII–>VIIIa (increase activity of IXa in intrinsic pathway)

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39
Q

Which pathway is the contact activation pathway?

A

intrinsic pathway

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40
Q

What pathway is the tissue factor pathway?

A

extrinsic pathway

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41
Q

Where do the two pathways connect?

A

At Xa where prothrombin is turned into thrombin

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42
Q

Warfarin can act on which parts of the pathway?

A

IIa VII, IX, X ( thrombin= IIa)

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43
Q

How does unfractionated heparin interfere on the pathway?

A

since it is longer, it has arms that can wrap around Xa and thrombin at the same time

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44
Q

Why does low-molecular weight heparin only bind to Xa and not thrombin?

A

it is shorter and can only wrap around the xa portion

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45
Q

What are side effects of heparin?

A

BLEEDING- thrombocytopenia

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46
Q

You should not give heparin if:

A

There is active bleeding
They are preparing for a surgery
renal dysfunction -low weight

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47
Q

What is the antidote for heparin?

A

protamine sulfate

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48
Q

What does DOAC’s stand for?

A

Direct Acting Oral Anticoagulants

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49
Q

What are three examples of DOAC’s?

A

Diabigatran
Rivaroxiban
Apixaban

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50
Q

What part of the pathway does Rivaroxiban and Apixaban work on?

A

Xa

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51
Q

What lab test are needed when on Warfarin?

A

PT- Prothrombin Time

INR- international normalized ratio

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52
Q

What are some vitamin K rich foods?

A

Avocados, kale, cabbage, kiwi, cucumber, celery, green beans, green pears
** must eat regularly and in moderation**

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53
Q

What is the role of erythropoietin?

A

Helps you make RBC

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54
Q

Erythropoientin (Procrit, EPOgen)

A

SC or IV
used to stimulate RBC formation- renal disease or oncologic/hematologic diseases
Must also have all other things to make RBCs

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55
Q

What are essential in RBC formation?

A

Iron, folic acid, B12, healthy bond marrow

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56
Q

What is the best way to treat iron deficiency anemia?

A

increase iron intake

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57
Q

Ferrous Sulfate

A

GI upset: nausea, heartburn, CONSTIPATION, diarrhea, stool can be dark green or black
TOXIC: in large doses, death common in peds- treat with deferoxamine
Interactions: Decreased with antacids, increased with vit C (but also increased AE)

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58
Q

Iron Dextran

A

parenteral iron product

AE: anaphylactic reactions (from dextran component), hypotension, circulatory failure, cardiac arrest.

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59
Q

VitaminB12 prep cyanocobalamin

A

purified crystalline form
AE: hypokalemia due to increased erythrocyte production
never given IV must be deep IM or SC

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60
Q

Folic Acid

A

Oral or IV

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61
Q

What is the definition of Relative anemia?

A

Normal total RBC mass, with increased plasma volume

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62
Q

What is an example of when someone would have relative anemia?

A

Pregnancy

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63
Q

What is absolute anemia?

A

decreased in RBC number

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64
Q

How are anemias classified?

A

Size and color
or
decreased RBC production, inherited disorders, destruction or loss

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65
Q

When you have a folic acid deficite, what will that result in?

A

premature cell death

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66
Q

When you are iron deficient, what will it result in?

A

lack of hemoglobin

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67
Q

What is aplastic anemia?

A

bone marrow suppression which leads to decreased production

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68
Q

What is claudication?

A

pain in muscles with exercise, normally due to lack of O2 in tissues

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69
Q

Clinical manifestations of anemia are categorized into what 3 groups?

A

mild, mild to moderate, moderate to severe

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70
Q

Why are manifestations divided based on characteristics and not actual numbers?

A

every body is different and tolerance can play a role, so people may not have the same response

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71
Q

What are examples of mild to moderate anemia?

A

fatigue, generalized weakness, tachy, loss of stamina, exertional dyspnea

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72
Q

What are examples of moderate to severe anemia?

A 
orthostatic/gen hypotension, 
vasoconstriction and palor
tachy, dyspnea
intermittent claudication
night cramps in muscles
headache, lightheadedness and fainting
roaring in ears
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73
Q

What are some evaluations that would be done for anemia?

A

hemoglobin/ hematocrit

bone marrow aspiration

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74
Q

What are some treatments for anemia?

A

Erythropoieten
transfusions
supplements
rest, O2, fluids (sickle cell)

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75
Q

What is something to keep in mind about anemia, in relation to chidren?

A

Sometimes milk can cause underlying problems, such as GI issues and blood loss-anemia

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76
Q

What is pica?

A

The craving to eat non-nutrative or nonfood items

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77
Q

What type of anemia is the most common?

A

Iron deficiency

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78
Q

What are some assessment findings for someon with iron deficient anemia?

A

PIca
fatigue
palor
microcytic, hypochromatic- pale/washed out

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79
Q

What is the most common treatment for iron deficient anemia?

A

oral administration

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80
Q

What is the etiology of iron deficiency ?

A

1- body can’t absorb it
2- the requirements for it have increased
3- excessive iron loss/blood loss
4- renal issues

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81
Q

What are 3 categories of bleeding disorders?

A

1- Vascular disorders
2- Platelet disorders
3- Coagulation Disorders

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82
Q

vascular purpura is an example of what type of bleeding disorder?

A

Vascular

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83
Q

Thrombocytopenia is an example of what type of bleeding disorder?

A

Platelet

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84
Q

What are some examples of coagulation disorders?

A

Vit K deficiency
inherited- hemophilia
DIC- disseminated intravascular coagulation

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85
Q

What is hemostasis?

A

The physiologic process that stops bleeding at the site of injury while maintaining normal blood flow elsewhere.

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86
Q

What is primary hemostasis?

A

VAsospasm at site of injury—-platelet plug- adhere and clump
3-7 mins

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87
Q

What is secondary hemostasis?

A

coagulation- formation of clot made of fibrin
clotting activation, clotting retraction=firming
can take up to an hour

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88
Q

What are the two pathways in the clotting cascade?

A

intrinsic- blood in contact with altered endothelium

extrinsic- tissue trauma

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89
Q

When assessing skin, what is one important thing to note?

A

Does it blanch?

90
Q

What is purpura?

A

patches of patechia

91
Q

What is Ecchymosis?

92
Q

What is hemarthrosis?

A

blood in joints

93
Q

What is hematochezia?

A

blood in stool

94
Q

What is epistaxis?

A

nose bleed

95
Q

Why would CBCs be taken for a lab value?

A

to look at platelet numbers and morphology of platelets

96
Q

Why would bleeding time be a test?

A

evaluate platelet and vascular response

97
Q

What do prothrombin (pt) and INRs test?

A

the EXTRINSIC pathway of coagulation

98
Q

What does an activated partial thromboplastin time (aPTT) test?

A

evaluates INTRINSIC pathway of coagulation

99
Q

What are some treatments for bleeding disorders?

A 
avoid the cause ie: meds, milk
Steroids- prevents platelet breakdown
IVIG- shirt term- prevents major bleeds
Factor replacement
Platelets 
Fresh frozen plasma
100
Q

What is thrombocytopenia?

A

generlized bleeding

101
Q

What is the cause of thrombocytopenia?

A

decreased production or increased consumption of platelets

102
Q

During an assessment, what would you see if someone had thrombocytopenia?

A

petechia, purpura, decreased platelet counts, bleeding

103
Q

how do you treat thrombocytopenia?

A

remove cause
block immune response
blood/platelet transfusion

104
Q

What is a thrombus?

A

stationary blood clot

in vessel or chamber of heart

105
Q

What is a thrombus composed of?

A

Aggregated platelets, clotting factors and fibrin that adhere to vessel wall

106
Q

What is Virchow’s Triad composed of?

A

Epithelial injury (vessel wall injury)
Circulatory Stasis
Hypercoagulable conditions

107
Q

What is DVT?

A

a thrombus in one of the deep veins

108
Q

What is the Virchow’s Triad giving risk factors for?

109
Q

What is an example circulatory stasis that can cause DVT?

A

bed bound, long flights

110
Q

What is an example of hypercoagulability that can cause DVT?

A

pregnancy, oral contraceptives, chemo, obesity

111
Q

What are examples of epithelial injury that can cause DVT?

A

trauma, IV, caths, smoking, hypertension, surgery

112
Q

What are the signs of DVT that you would see on a patient in assessment?

A

edema
pain/tenderness
redness, discoloration
warmth

ultrasound, D-dimer lab

113
Q

What is the treatment for DVT?

A

a thrombalytic to break down the clot

Anticoagulant to reduce further clot formation

114
Q

How do you prevent DVTs?

A

MOVE
Anticoagulants
SCD or compression socks
good hydration

115
Q

What re the 3 things that cells do when presented with a problem?

A

1-withstand and return to normal
2- adapt
3- die

116
Q

What are two types of reversible cell damage?

A

Hydropic and cellular accumulations

117
Q

What are 5 types of cell damage that are generally reversible?

A 
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
118
Q

What are the two types of cell death?

A

Necrosis

Apoptosis

119
Q

What is Hydropic cell damage?

A

Accumulation of water.-
malfunction of Na-K pump- Na in cell-water follows
*normally first manifestation of most forms of reversible damage

120
Q

What does megaly mean?

A

generalized swelling of cells for certain organ- enlargement

121
Q

What are three parts to intracellular Accumulations?

A

1- excessive amounts of normal substances
2- Accumulation of abnormal- produced by cell
3- Accumulation of pigments and particles- unable to degrade

122
Q

What is an example of intracellular accumulation from excessive amounts of normal substances?

A

Diabetes- body does not break down glucose

Fatty deposits in liver

123
Q

What is an example of intracellular accumulation from abnormal substances produced by cell?

124
Q

What is an example of intracellular accumulation from pigments and particles?

A

Hyperbillirubanemia

125
Q

What is Atrophy and what happens to the cell?

A

Cells shrink & reduce differentiated function

-conserves energy for the body

126
Q

What are some examples of why Atrophy would happen?

A

No use- fractires, bedbound, eschemia, starvation

127
Q

What is Hypertrophy and what does it do to the cells?

A

Increase in cell size
WITH augmented functional capacity
cells are working harder
** could increase BP which could lead to CHF

128
Q

What are some examples of hypertrophy would happen?

A

Pregnancy - enlargement of uterus and breasts

129
Q

What is Hyperplasia?

A

Increase in NUMBER of cells through mitotic division

130
Q

What is Metaplasia?

A

Replacement of one differentiated cell type with another

swap out

131
Q

What is an example of when Metaplasia would happen?

A

Smoking- bronchial mucosa changes

132
Q

What is Dysplasia?

A

Disorganized appearance of cells because of abnormal variations

133
Q

What are some reasons cell injury occurs?

A 
Ischemia
Hypoxia
Infections
Chemical
Physical
134
Q

What can Ca overload cause?

A

apoptosis of cells

135
Q

What are two reasons Ca overload could happen and why?

A

Hypoxia and Ischemia

-ATP made-pumps fail- H2O & Na–>excess Ca

136
Q

What are examples of chemical cell injuries?

A

Free redicals
Heavy metals
Toxic gasses

137
Q

What are some nutritional examples of cell injury?

A 
Malnutrition
low iron
increased sodium
obesity
diabetes
138
Q

What are some examples of physical and mechanical cell injury?

A 
temp changes
abrupt atmoshperic pressure change
Abrasion
Electrical
Radiation
139
Q

Whtat are some infectious and immunological examples of cell injury?

A

Bacteria- endo/exo toxins
Virus
indirect immunologic response

140
Q

What are the clinical manifestations of hyponatremia?

A

CNS dysfunction
Malaise, anorexia, nausea, vomiting, HA
confusion, lethargy, seizures, coma
fatal cerebral herniation

141
Q

What are clinical manifestations of hypernatremia?

A 
Thirst, dry mucous membranes
hypotension, tachy
Oliguria
Muscle irritation
agitation
Confusion, lethargy, seizures, coma, death
142
Q

What are the clinical manifestations of Hypokalemia?

A 
hyperpolarized smooth and skeletal muscles- less reactive
Abd distension, no bowel sounds
postural hypotension
skeletal musces weakness, paralysis
cardiac dysrhythmia
143
Q

What are the clinical manifestations of Hyperkalemia?

A

hypopolarized smooth/skeletal muscles- can’t fire after discharge
intestinal cramping and diarrhea
skeletal muscle weakness, paralysis
cardiac dysrhythmia and arrest

144
Q

What are the clinical manifestations of hypocalcemia?

A

Increased neurotransmuscular excitability- twitching, cramping, hyperactive reflexes, tetany
seizures, dysrhythmias

145
Q

What are the clinical manifestations of hypercalcemia?

A

Anorexia, nausea, emesis, constipation, fatigue, muscles weakness, diminished reflexes, HA, confusion, lethargy,
heart block, brady
kidney stones

146
Q

What is ROME?

A 
Respiratory= opposite moving numbers
Metabolic= Same moving numbers
147
Q

What are the clinical manifestations of respiratory acidosis?

A

HA, tachy, cardiac dsy
blurred vision, tremors, vertigo, disorientation, lethargy

**INCREASED PaCO2 DECREASED pH

148
Q

What are the clinical manifestations of respiratory alkalosis?

A

numbness, tingling, feet/hand spasms
confusion, cerebral vasoconstriction
DECREASED PaCO2. INCREASED pH

149
Q

What are clinical manifestations of metabolic acidosis?

A 
GI upset- N/V/D
dehydration
lethargy, stupor coma
tachy, dysrhythmia
fruity breath
DECREASED bicorbonate and pH
150
Q

What are clinical manifestations of metabolic alkalosis?

A 
GI- N/V/D
tingling, tetany, seizures
hypokalemia
bilateral muscles weakness
irritability CNS depression
INCREASE bicarb and pH
151
Q

What are the 4 drugs used for treatment of hyperkalemia?

A

Albuterol
Dextrose 50% injection
Insulin, regular
Kayexalate

152
Q

What is the most common type of potassium supplement?

A

Potassium chloride

153
Q

What would be a good reason to use potassium phosphate?

A

If they lack potassium and phosphate

154
Q

Why is potassium given?

A

most commonly for hypokalemia

155
Q

What are the two forms potassium comes in?

A

liquid or powder

** IV sight can be irritated or painful

156
Q

Potassium side effects

A

GI: N/V/D abd discomfort
esophagitis
**give with food

157
Q

What levels will you need to watch when giving potassium chloride?

A

1- serum K levels
2- watch for hyperkalemia
3- watch IV site

158
Q

What are some contraindications for potassium chloride?

A

Renal dysfunction? **monitor very close!

watch close for those already taking meds that could increase serum K levels

159
Q

What type of IV can you use for K?

A

Central or peripheral
** watch close for irritation and pain
can be added to maintenance IV fluid

160
Q

Concentrated potassium…

A

should never be available on patient care units

161
Q

What are the two approaches for treatment of hyperkalemia?

A

1- Shift K back into cell

2- Increase excretion of K

162
Q

What would you use to stabilize the heart with hyperkalemia?

A

Calcium IV

163
Q

What would you use to shift K back into the cells?

A

Insulin and dextrose 50% injection
Sodium bicarb injection
Albuterol inhalation

164
Q

For increasing excretion of K, what are the three options?

A

using the kidneys- diuretics **always know underlying cause
Fake kidney- hemodialysis
Use gut- Sodium polystyrene

165
Q

What are the two types of IV Calcium?

A

Calcium gluconate

Calcium chloride

166
Q

What is the equation of the two types of calcium?

A

3g Gluconate= 1g Chloride

167
Q

How would you give calcium gluconate?

A

Peripherally

168
Q

How would you give calcium chloride?

169
Q

If you are giving calcium for Hyperkalemia, what rate would you give it?

A

10-30 mins 2g- immediate

170
Q

If you are giving calcium for hyokalemia/replacement, how fast would you give it?

A

slow- 1g hr just to keep it in there

171
Q

What does the Na-K ATP pump do?

A
  • Maintains intracellular and extracelluar K concentrations
  • Exchanges Na for K in 3:2 ratio
  • Enhances movement of K into cells
172
Q

What is required for the ATP pump to work?

A

Insulin and glucose AKA dextrose

*must have the insulin to have glucose uptake

173
Q

What would you check for when giving insulin?

A

CBG levels

174
Q

When giving sodium bicorbonate, what do you need to watch for?

A

Edema, potassium levels

175
Q

Why would you use sodium bicarb?

A

for severe metabolic acidosis, hyperkalemia
**this is just a bandaid
- sometimes used for OD
overcorrection happens

176
Q

What are the adverse effects of sodium bicorbonate?

A

caustic to vasculature, can cause hypokalemia, can cause metabolic alkalosis

177
Q

Albuterol

A

inhalant- Beta2 agonist
brochodilation
-activates cAMP–> helps move K intracellularly

178
Q

What is a side effect of albuterol?

A

Tachycardia

179
Q

Kayexalate: sodium polystyrene

A

resin that exchanges Na for K in gut *NOT absorbed
Oral/Rectal
*not for emergencies, few hour onset

180
Q

What are some serious AE of Kayexalate?

A

intestinal necrosis/ other serious GI problems

181
Q

What doe magnesium do in the body?

A

activates intracellular enzymes
binds to mRNA to ribosomes
helps regulate muscle contractility/ blood coag

182
Q

What are the two types of mag replacement? how is it given?

A

mag sulfate- IV

mag oxide- Oral, over several days

183
Q

Why would you give mag sulfate?

A

preeclampsia
migraines
status asthmaticus
hypomagnesemia

184
Q

What is Capillary hydrostatic pressure?

A

In capillary pushing out into interstitial space

185
Q

What is Capillary Oncotic pressure?

A

in capillary pulling in water from interstitial space

186
Q

What is Interstitial hydrostatic pressure?

A

in interstitial space pushing into capillary

187
Q

What is interstitial oncotic pressure?

A

in interstitial space pulling back from capillary

188
Q

What is the definition of edema and hypervolemia?

A

excessive accumulation of fluid within interstitial space

189
Q

What are the forces that are involved with edema and hypervolemia?

A

Increased Capillary Hydrostatic pressure
Increased cap permeability
decreased plasma oncotic pressure
Lymphatic channel obstruction

190
Q

What is an example of why someone would have decreased plasma oncotic pressure?

A

malnutrition, burns, kidney disease

191
Q

What is an example of why someone would have increased capillary perm?

A

inflammation or immune response

192
Q

What is an exampe of why someone would have increased cap. hydrostatic pressure?

A

kidney failure or heart failure

193
Q

What is an example of why someone would have lymphatic channel obstruction?

A

Removal of lymphs

inflammatory process

194
Q

What is localized edema?

A

limited to one site of trauma or with a particular organ system

195
Q

What is generalized edema?

A

uniformed distribution. normally in dependent areas b/c of gravity
ex/ legs

196
Q

What are some clinical manifestations of edema you would see?

A

weight increase, swelling, puffiness, limited movement, crackles, respiratory distress, bounding pulse, tachy

197
Q

What are 4 ways to treat Edema?

A

Treat underlying cause
be supportive and educate
CHange diet- low sodium
Diuretics

198
Q

What is the definition of clinical dehydration and hypovolemia?

A

too small amount of fluid in extracellular compartment.

fulids are too concentrated

199
Q

What are three reasons why someone would have hypovolemia?

A

Fluid loss- burns, emesis, hemorrhage. sweating, diabetes
Reduced intake- altered cog. dependence
Fluid shifts- burns

200
Q

What are some clinical manifestations for hypovolemia?

A 
poor skin turger, tachy, hypotension
dry mucous
weight loss, crying with no tears
dark urine/less urine
thirst
201
Q

How would you treat hypovolemia?

A

stop the reason they are losing the fluid

give fluids- slowly. too fat can cause cerebral hyervolemia

202
Q

What is the normal range of K?

203
Q

What is the normal range for sodium?

204
Q

What is the normal range for Phosphate?

205
Q

What is the normal range for magnesium?

206
Q

What is the normal range for calcium?

A

9-11mg/dl 4.5-5.5 mEq/L

207
Q

What are the main roles of Na?

A

Regulates acid-base balance
Nerve conduction and neuro- muscular function
Maintains water balance

208
Q

What are some reasons people have have hyponatremia?

A 
Inappropriate fluid admin
Tap water ememas
Excess of ADH (antiduiretics)
Too many diuretics
Renal disease
209
Q

What are some reasons someone would have hypernatremia?

A 
Tube feedings
Overuse of salt
No access to water
Emesis
Diarrhea
210
Q

What is the role of K in body?

A

Maintain Electricaly Neutrality
Cardiac muscle contraction
Neuromuscular/ nerve impulses
Acid-base balance

211
Q

What are some reasons that someone would be hypokalemic?

A 
NPO
Fasting
Fad diet
Anorexia
Alkolosis
Diuretics, diarrhea, emesis, gastric succ.
212
Q

What are some reasons that someone would be hyperkalemic?

A 
blood transfusions
acidosis
crushing injury
meds
olguria
213
Q

What is the role of Ca in the body?

A

Blood coag
Nerve impulses
Muscle contractions
Cardiac action potential

214
Q

What are some reasons someone would be hypocalemic>

A 
Kidney disease
Diet
Diarrhea
Alkalosis 
Pancreatitis- (fatty stools)
215
Q

What are some reasons someone would be hypercalemic?

A

tumors
leukemia
immobilized
diuretics

216
Q

What is the normal range for PaCO2?

A

36-44 mm Hg

217
Q

What are the normal ranges for HCO3-?

A

22-26 mm Hg

218
Q

What are some causes of respiratory acidosis?

A 
pneumonia
asthma
COPD
chest injury/surgery
meds/drugs
219
Q

What are some causes of Respiratory alkalosis?

A 
Hyperventilation
anxiety
brainstem injury
panic attacks
crying
acute pain
hypoxemia
220
Q

What are some causes of metabolic acidosis?

A

ketoacidosis, diabetes
burns
circulatory shock
Diarrhea

221
Q

What are some causes of metabolic alkalosis?

A 
over use of antacids
hypovolemic
emesis
hypokalemia
diuretics

Pharm/Patho (6 decks)

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