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Pharmacology 1 > FInal > Flashcards

FInal Flashcards

1
Q

what do cells use as a source of energy

A

glucose

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2
Q

What hormone increases the amount of glucose in the blood

A

glucagon

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3
Q

What hormone decreases the amount of glucose in the blood

A

insulin

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4
Q

what produces insulin?

A

beta cells in the pancreas

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5
Q

difference between DM T1 and T2

A

T1 - absolute insulin insufficiency

T2 - insulin resistance & decreased secretion

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6
Q

what causes DM T1

A

autoimmune attack on the beta cells of the pancreas

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7
Q

Etiology of DMT1

A

peak onset 11-13 years
rates are higher for whites
accounts for 5-10% of DM

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8
Q

how many beta cells are destroyed by the time s/sx are present?

A

90%

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9
Q

clinical manifestations of DMT1

A

Polyuria; excessive urination
Polydipsia: excessive thirst
Polyphagia: excessive hunger/eating

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10
Q

patho of polyuria

A

There is too much blood sugar for the kidneys to pull back in. Glucose goes into the urine and water follows

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11
Q

patho of polydipsia

A

hyperglycemia causes changes in the brain which triggers thirst

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12
Q

patho of polyphagia

A

insulin is not maintaining the metabolic demands of the cells

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13
Q

clinical manifestations of both DMT1 and T2

A

slow healing and tingling

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14
Q

Blood glucose levels

A

Random sampling of blood glucose above 200 mg/dl with classic signs and symptoms

Fasting blood glucose level of greater than 126 mg/dl

Blood glucose concentration greater than 200 mg/dl 2 hours after a 75-g oral glucose load

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15
Q

HbA1C level

A

above 6.5

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16
Q

True or False

both DM T1 and T2 will have ketones present in the urine

A

False. Only T1

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17
Q

Treatment for DMT1

A 
insulin therapy
diet/meal planning
activity/exercise
glucose monitoring 
monitoring for complications
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18
Q

Symptoms of Hypoglycemia

A 
TIRED
tachycardia
irritable 
restless 
excessive hunger 
diaphoresis/depression
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19
Q

causes of diabetic ketoacidosis

A

prolonger period without insulin. Compliance with medication (sick). Emotional Stress, Accidents, Trauma

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20
Q

Clinical symptoms of diabetic ketoacidosis

A

deep, labored respirations, increased RR, smelly breath (juice fruit), thirsty, hypotension, hyperkalemia

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21
Q

T or F

the most common type of DM is T1

A

false. it is T2

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22
Q

who does DMT2 affect the most

A

American Indian, Alaskan Natives

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23
Q

who does DMT2 affect the least

A

non-white hispanics

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24
Q

risk factors of DMT2

A

hypertension, obesity and physical inactivity

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25
Q

difference between evaluation of T1 and T2

A

T1 will have ketones in urine

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26
Q

treatment for DMT2

A

diet, exercise, weight loss, medications (oral, insulin over time)
monitoring for complications

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27
Q

complications for T1 and T2

A

eyes - loss of visual acuity, loss of central vision, blurring cataracts
cardiovascular - hypertension, coronary artery disease and risk of heart failure
kidneys - end stage kidney failure
cerebrovascular - ischemic and thrombotic stroke
neuropathy - sensation changes
peripheral vascular - poor profusion, pain, ulcers that doesn’t heal, gangrene
infection - wound healing

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28
Q

clinical manifestations for both T1 and T2

A

slow healing, tingling

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29
Q

what is gestational diabetes?

A

glucose intolerance developed during pregnancy

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30
Q

risk factors for gestational diabetes

A

older age, family history, severe obesity, previous history of GDM, previous children who were more than 9 lbs. at birth, strong family history of T2DM

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31
Q

when are pregnant persons screened for GDM?

A

28 weeks

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32
Q

how are pregnant persons screened for GDM?

A

glucose tolerance test

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33
Q

treatment for GDM

A

glocose monitoring
nutritional counseling and exercise
insulin if not controlled with above

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34
Q

complications from GDM

A

macrosomia (big baby)
neonatal hypoglycemia
still birth (fetal demise)

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35
Q

T or F; pregnant persons with GDM have a higher chance of developing DM in next 10-20 years?

A

True

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36
Q

Addison Disease is caused by what?

A

destruction of adrenal cortex, decreased secretion of mineralocorticoids, glucocorticoids and androgens

removal of adrenal gland
neoplasms
tuberculosis, histoplasmosis, cytomegalovirus
autoimmune disease

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37
Q

what is a primary Adrenocortical Insufficiency?

A

Addison’s disease

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38
Q

Ulcerative Colitis

A

Inflammatory disease of the mucosa of the colon and rectum

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39
Q

what are clinical manifestations of ulcerative colitis?

A

Progression is variable
what you see in one you might not see in another
diarrhea
abdominal pain, cramping, urge to defecate
can see signs and symptoms elsewhere

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40
Q

Diagnosis and Treatment of Ulcerative Colitis and Crohn’s

A

history and physical
biopsy / endoscopy
corticosteroids, immunosuppressants, immunomodulating agents, nutritional management, antibiotics if systemic toxicity, risk for colon cancer increases due to inflammatory process

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41
Q

what is the nutritional management for ulcerative colitis?

A

avoid milk, hypoallergenic diet, low fiber, low fat, low residue, high protein

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42
Q

Crohn’s disease

A

inflammation of the GI tract that extends through all layers of the intestinal wall - mouth to anus

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43
Q

what are cardinal features of Crohn’s disease?

A

granulomas (cobblestone)

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44
Q

Clinical manifestations of Crohn’s disease

A

incapable of adequately absorbing (malnutrition)

diarrhea, weight loss, abdominal pain, don’t see bleeding, “skipping lesions” perianal fissures

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45
Q

Nutritional management for Crohn’s

A

broad nutritional support, protein, fat, carbs, vitamins, related to malnutrition

46
Q

GERD

A

back flow of gastric contents into the esophagus through the lower esophageal sphincter

47
Q

what the 3 broad causes of GERD

A

Issues with LES: closure and efficacy
increase in intraabdominal pressure (pregnancy, crying, pooping, vomiting, coughing)
delayed gastric emptying (gastric, ulcers)

48
Q

risks for GERD

A

age, obesity, medications, pregnancy

49
Q

Clinical manifestations for GERD

A

no symptoms (physiologic reflux)
heartburn (chest pain)
regurgitation
dysphasia

50
Q

Evaluation of GERD

A

history and physical
endoscopy
pH monitoring

51
Q

Treatment of GERD

A

dietary and behavior modifications
antacids and histamine blockers
proton pump inhibitors
limit fatty food, alcohol, caffeine, serving sizes are appropriate, not eating right before bed

52
Q

true or false: reflux is normal in newborns

A

true

53
Q

GERD is highest in premature infants and decreases during first 6-12 months

A

true

54
Q

Would neurologic impairment affect GERD? If yes, what?

A

yes and CP, downs, head injury

55
Q

treatment of GERD in pediatric patients

A

small, frequent feedings & burping
thickened feeding controversial (might not help GERD, but helps QOL of parents)
positioning
medications

56
Q

Symptoms of GERD in peds

A 
feeding refusal
recurrent vomiting 
poor weight gain
irritability 
sleep disturbances
respiratory symptoms
abdominal pain/heartburn
recurrent vomiting
dysphagia
asthma 
recurrent pneumonia 
upper airway symptoms (chronic cough, hoarse voice)
57
Q

what is a fracture?

A

break in continuity of a bone, an epiphyseal plate or cartilaginous joint surface

58
Q

who are the risk groups for fractures?

A

older and younger. Typically makes between 15-24

59
Q

what are difference in pediatric bones?

A

less brittle, higher collagen to bone ratio (can absorb more of the trauma)
stronger periosteum
presence of epiphyseal plate (weakest part of the bone)

60
Q

clinical manifestations of fractures

A 
pain
swelling
warmth
bruising
restriction of movement
muscle spasms
deformity
impaired sensation
61
Q

diagnosis & treatment of fractures

A 
history and physical 
2 sets of x-rays (repeat in 1-2 weeks)
ice & elevation 
reduction (realignment)
immobilization / Retention (splint/cast)
62
Q

what might delay healing of a fracture?

A

smoking, nutrition, corticosteroids (blocks inflammation), elderly, comorbid disease (diabetes)

63
Q

what is a malunion fracture

A

improperly aligned

64
Q

what is a nonunion fracture

A

not healed after 6 months

65
Q

Osteonecrosis

A

tissue has dead bone

66
Q

Compartment Syndrome

A 
Accumulation of pressure and there is constriction.  Surgical emergency.
5 Ps 
pain out of proportion
paralysis 
paresthesia
pallor 
pulselessness
67
Q

Fat emboli syndrome

A

fat gets into circulatory system

68
Q

Osteomyelitis

A

severe infection of bone and local tissue

69
Q

How can an infection reach the bone?

A

bloodstream
adjacent soft tissue
direct introduction of the organism into the bone

70
Q

who are at high risk for osteomyelitis?

A 
under 16
elderly 
IV drugs users 
patients with indwelling lines
trauma 
surgery
71
Q

clinical manifestations of osteomyelitis

A 
acute vs chronic 
pain
high fever
redness 
swelling
muscle spasms 
refusal to move limb
72
Q

Osteomyelitis diagnosis

A

X-ray (longer to show up
increased WBC, CRP, ESR (tell us there is an infection or inflammation) markers to determine if things are improving
bone scan/MRI
blood cultures or bone aspirate

73
Q

treatment of osteomyelitis

A

4-6 weeks of IV antibiotics OR
IV then switch to PO
debridement if needed (surgery)
removal of prosthesis or other materials

74
Q

what is significant about an epiphyseal fracture?

A

can separate the plate from the rest of the bone that is trying to grow

75
Q

5 stages of bone healing

A
  1. bleeding at the end of the bone
  2. hematoma responsible for fibrous network will support development of new bone growth
  3. osteoblasts are sent and are responsible for building new bone. Will show up on X-ray
  4. Osteoblast & Osteoclast (reabsorbing the old bone and helping to clean up old bone)
  5. excess callus is reabsorbed and final mature bone is created
76
Q

what is the ductus arteriosous?

A

shunts blood from pulmonary artery to aorta – skips lungs

77
Q

what is the foramen ovale?

A

shunts blood from RA to LA (atrium) – skips lungs

78
Q

what heart defects falls into the category of increased pulmonary blood flow?

A

Patent Ductus Arteriosus (PDA)
Ventricular Septal Defect
Atrial Sepal Defect

79
Q

what heart defect falls into the category of obstruction to blood flow

A

Coarctation of Aorta

80
Q

what heart defect falls into the category of decreased pulmonary blood flow

A

Tetralogy of Fallot

81
Q

what heart defect falls into the category of mixed blood flow?

A

Transposition of great arteries

82
Q

what is the defect of PDA?

A

open ductus arteriosus

83
Q

what is the pathophysiology of PDA?

A

shunt doesn’t close, remains open (24-72 hours should close on its own)

84
Q

what sided heart failure does PDA cause?

A

right sided. Extra workload is on the right side

85
Q

clinical manifestations of PDA

A 
Asymptomatic
HF
murmor 
widened pulse pressure
bounding pulses 
cardiac enlargement
86
Q

what is the defect of atrial septal defect?

A

opening b/w R and L atrium (usually at place of foremen novale)

87
Q

what sided heart failure does ASD cause?

A

right sided. Blood going from LA to RA

88
Q

Clinical manifestations of ASD

A 
depends on size-small (asymptomatic) large (CHF)
fatigue
dyspnea on exertion
recurrent resp infections
murmur 
HF develop in young adulthood
89
Q

what is the defect in Ventricular Septal Defect?

A

opening b/w R and L ventricles

90
Q

what sided HF does VSD cause?

A

right sided. Blood goes from LV to RV

91
Q

what is the most common congenital heart defect?

A

VSD

ventricular septal defect

92
Q

clinical manifestations of VSD?

A

related to size of defect
murmur
heart failure

93
Q

what is the defect of coarctation of aorta?

A

narrowing of aorta. Obstructing blood flow to the body

94
Q

Clinical manifestations of coarctation of aorta

A

murmur
poor lower extremity peripheral perfusion
pulse and BP difference in upper and lower extremities
left sided HF

95
Q

Defect of Tetralogy of Fallot

A

VSD, pulmonary stenosis (narrowing), overriding aorta (taking blood from both RV and LV), R ventricular hypertrophy

96
Q

What side if tetralogy of fallot affecting?

A

right side. blood is not getting to the lungs

97
Q

clinical manifestations of tetralogy of fallot

A 
severity directly related to pulmonic stenosis
becomes worse after DA closes 
cyanosis, fatigue
hyper-cyanotic episodes
murmur
boot shaped heart on x-ray
98
Q

what are triggers from hyper-cyanotic tet spells

A

crying, pooping, feeding, fever, dehydration

99
Q

defect of transposition of great arteries

A

aorta & pulmonary artery are switched. 2 closed, non-communicating circuits

100
Q

what are the two defects that are cyanotic?

A

tetralogy of fallot

transposition of great arteries

101
Q

clinical manifestations of transposition of great arteries

A

cyanosis at birth
hypoxemia with O2
progressive desaturation and acidosis
heart failure

102
Q

what is heart failure

A

inability to heart maintain sufficient cardiac output to meet metabolic demands of tissues and organs

103
Q

common causes for heart failure

A

myocardial ischemia
hypertension
cardiomyopathy

104
Q

clinical manifestations of left sided heart failure

A 
dyspnea 
orthopnea (shortness of breath while lying down)
cough, crackles
hemoptysis 
tachycardia 
cool, pale skin
105
Q

clinical manifestations of right sided heart failure

A

jugular vein distention
hepato-splenomegaly
weight gain, edema

106
Q

treatment for congestive heart failure

A

manipulate preload, after load & contractility
improve cardiac output
minimize congestive symptoms
minimize cardiac workload

107
Q

what is the most common complication of many congenital heart defects in pediatrics?

A

congestive heart failure

108
Q

CHF in pediatrics is most often the result of what?

A

decreased left ventricular systolic function

109
Q

treatment of CHF in pediatrics

A 
treat underlying cardiac defect
fluid balance (increase calorie content of feedings, diuretics)
increase cardiac output
110
Q

The 3 compensatory mechanisms that are triggered in heart failure work to restore cardiac output

A

baroreceptor response-SNS activation-increased HR and increase contractility
RAAS activation Decreased GFR-fluid retention-increase preload
Increase ventricular wall tension-myocyte growth-hypertrophy

111
Q

Heart failure classifications - systolic

A

ventricles don’t pump enough blood out

112
Q

heart failure classifications - diastolic

A

ventricles don’t fill properly

Pharmacology 1 (3 decks)

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