FInal Flashcards
1
Q
what do cells use as a source of energy
A
glucose
2
Q
What hormone increases the amount of glucose in the blood
A
glucagon
3
Q
What hormone decreases the amount of glucose in the blood
A
insulin
4
Q
what produces insulin?
A
beta cells in the pancreas
5
Q
difference between DM T1 and T2
A
T1 - absolute insulin insufficiency
T2 - insulin resistance & decreased secretion
6
Q
what causes DM T1
A
autoimmune attack on the beta cells of the pancreas
7
Q
Etiology of DMT1
A
peak onset 11-13 years
rates are higher for whites
accounts for 5-10% of DM
8
Q
how many beta cells are destroyed by the time s/sx are present?
A
90%
9
Q
clinical manifestations of DMT1
A
Polyuria; excessive urination
Polydipsia: excessive thirst
Polyphagia: excessive hunger/eating
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
11
Q
patho of polydipsia
A
hyperglycemia causes changes in the brain which triggers thirst
12
Q
patho of polyphagia
A
insulin is not maintaining the metabolic demands of the cells
13
Q
clinical manifestations of both DMT1 and T2
A
slow healing and tingling
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
15
Q
HbA1C level
A
above 6.5
16
Q
True or False
both DM T1 and T2 will have ketones present in the urine
A
False. Only T1
17
Q
Treatment for DMT1
A
insulin therapy diet/meal planning activity/exercise glucose monitoring monitoring for complications
18
Q
Symptoms of Hypoglycemia
A
TIRED tachycardia irritable restless excessive hunger diaphoresis/depression
19
Q
causes of diabetic ketoacidosis
A
prolonger period without insulin. Compliance with medication (sick). Emotional Stress, Accidents, Trauma
20
Q
Clinical symptoms of diabetic ketoacidosis
A
deep, labored respirations, increased RR, smelly breath (juice fruit), thirsty, hypotension, hyperkalemia
21
Q
T or F
the most common type of DM is T1
A
false. it is T2
22
Q
who does DMT2 affect the most
A
American Indian, Alaskan Natives
23
Q
who does DMT2 affect the least
A
non-white hispanics
24
Q
risk factors of DMT2
A
hypertension, obesity and physical inactivity
25
difference between evaluation of T1 and T2
T1 will have ketones in urine
26
treatment for DMT2
diet, exercise, weight loss, medications (oral, insulin over time)
monitoring for complications
27
complications for T1 and T2
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
28
clinical manifestations for both T1 and T2
slow healing, tingling
29
what is gestational diabetes?
glucose intolerance developed during pregnancy
30
risk factors for gestational diabetes
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
31
when are pregnant persons screened for GDM?
28 weeks
32
how are pregnant persons screened for GDM?
glucose tolerance test
33
treatment for GDM
glocose monitoring
nutritional counseling and exercise
insulin if not controlled with above
34
complications from GDM
macrosomia (big baby)
neonatal hypoglycemia
still birth (fetal demise)
35
T or F; pregnant persons with GDM have a higher chance of developing DM in next 10-20 years?
True
36
Addison Disease is caused by what?
destruction of adrenal cortex, decreased secretion of mineralocorticoids, glucocorticoids and androgens
removal of adrenal gland
neoplasms
tuberculosis, histoplasmosis, cytomegalovirus
autoimmune disease
37
what is a primary Adrenocortical Insufficiency?
Addison's disease
38
Ulcerative Colitis
Inflammatory disease of the mucosa of the colon and rectum
39
what are clinical manifestations of ulcerative colitis?
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
40
Diagnosis and Treatment of Ulcerative Colitis and Crohn's
history and physical
biopsy / endoscopy
corticosteroids, immunosuppressants, immunomodulating agents, nutritional management, antibiotics if systemic toxicity, risk for colon cancer increases due to inflammatory process
41
what is the nutritional management for ulcerative colitis?
avoid milk, hypoallergenic diet, low fiber, low fat, low residue, high protein
42
Crohn's disease
inflammation of the GI tract that extends through all layers of the intestinal wall - mouth to anus
43
what are cardinal features of Crohn's disease?
granulomas (cobblestone)
44
Clinical manifestations of Crohn's disease
incapable of adequately absorbing (malnutrition)
| diarrhea, weight loss, abdominal pain, don't see bleeding, "skipping lesions" perianal fissures
45
Nutritional management for Crohn's
broad nutritional support, protein, fat, carbs, vitamins, related to malnutrition
46
GERD
back flow of gastric contents into the esophagus through the lower esophageal sphincter
47
what the 3 broad causes of GERD
Issues with LES: closure and efficacy
increase in intraabdominal pressure (pregnancy, crying, pooping, vomiting, coughing)
delayed gastric emptying (gastric, ulcers)
48
risks for GERD
age, obesity, medications, pregnancy
49
Clinical manifestations for GERD
no symptoms (physiologic reflux)
heartburn (chest pain)
regurgitation
dysphasia
50
Evaluation of GERD
history and physical
endoscopy
pH monitoring
51
Treatment of GERD
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
true or false: reflux is normal in newborns
true
53
GERD is highest in premature infants and decreases during first 6-12 months
true
54
Would neurologic impairment affect GERD? If yes, what?
yes and CP, downs, head injury
55
treatment of GERD in pediatric patients
small, frequent feedings & burping
thickened feeding controversial (might not help GERD, but helps QOL of parents)
positioning
medications
56
Symptoms of GERD in peds
```
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
what is a fracture?
break in continuity of a bone, an epiphyseal plate or cartilaginous joint surface
58
who are the risk groups for fractures?
older and younger. Typically makes between 15-24
59
what are difference in pediatric bones?
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
clinical manifestations of fractures
```
pain
swelling
warmth
bruising
restriction of movement
muscle spasms
deformity
impaired sensation
```
61
diagnosis & treatment of fractures
```
history and physical
2 sets of x-rays (repeat in 1-2 weeks)
ice & elevation
reduction (realignment)
immobilization / Retention (splint/cast)
```
62
what might delay healing of a fracture?
smoking, nutrition, corticosteroids (blocks inflammation), elderly, comorbid disease (diabetes)
63
what is a malunion fracture
improperly aligned
64
what is a nonunion fracture
not healed after 6 months
65
Osteonecrosis
tissue has dead bone
66
Compartment Syndrome
```
Accumulation of pressure and there is constriction. Surgical emergency.
5 Ps
pain out of proportion
paralysis
paresthesia
pallor
pulselessness
```
67
Fat emboli syndrome
fat gets into circulatory system
68
Osteomyelitis
severe infection of bone and local tissue
69
How can an infection reach the bone?
bloodstream
adjacent soft tissue
direct introduction of the organism into the bone
70
who are at high risk for osteomyelitis?
```
under 16
elderly
IV drugs users
patients with indwelling lines
trauma
surgery
```
71
clinical manifestations of osteomyelitis
```
acute vs chronic
pain
high fever
redness
swelling
muscle spasms
refusal to move limb
```
72
Osteomyelitis diagnosis
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
treatment of osteomyelitis
4-6 weeks of IV antibiotics OR
IV then switch to PO
debridement if needed (surgery)
removal of prosthesis or other materials
74
what is significant about an epiphyseal fracture?
can separate the plate from the rest of the bone that is trying to grow
75
5 stages of bone healing
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
what is the ductus arteriosous?
shunts blood from pulmonary artery to aorta – skips lungs
77
what is the foramen ovale?
shunts blood from RA to LA (atrium) – skips lungs
78
what heart defects falls into the category of increased pulmonary blood flow?
Patent Ductus Arteriosus (PDA)
Ventricular Septal Defect
Atrial Sepal Defect
79
what heart defect falls into the category of obstruction to blood flow
Coarctation of Aorta
80
what heart defect falls into the category of decreased pulmonary blood flow
Tetralogy of Fallot
81
what heart defect falls into the category of mixed blood flow?
Transposition of great arteries
82
what is the defect of PDA?
open ductus arteriosus
83
what is the pathophysiology of PDA?
shunt doesn't close, remains open (24-72 hours should close on its own)
84
what sided heart failure does PDA cause?
right sided. Extra workload is on the right side
85
clinical manifestations of PDA
```
Asymptomatic
HF
murmor
widened pulse pressure
bounding pulses
cardiac enlargement
```
86
what is the defect of atrial septal defect?
opening b/w R and L atrium (usually at place of foremen novale)
87
what sided heart failure does ASD cause?
right sided. Blood going from LA to RA
88
Clinical manifestations of ASD
```
depends on size-small (asymptomatic) large (CHF)
fatigue
dyspnea on exertion
recurrent resp infections
murmur
HF develop in young adulthood
```
89
what is the defect in Ventricular Septal Defect?
opening b/w R and L ventricles
90
what sided HF does VSD cause?
right sided. Blood goes from LV to RV
91
what is the most common congenital heart defect?
VSD
| ventricular septal defect
92
clinical manifestations of VSD?
related to size of defect
murmur
heart failure
93
what is the defect of coarctation of aorta?
narrowing of aorta. Obstructing blood flow to the body
94
Clinical manifestations of coarctation of aorta
murmur
poor lower extremity peripheral perfusion
pulse and BP difference in upper and lower extremities
left sided HF
95
Defect of Tetralogy of Fallot
VSD, pulmonary stenosis (narrowing), overriding aorta (taking blood from both RV and LV), R ventricular hypertrophy
96
What side if tetralogy of fallot affecting?
right side. blood is not getting to the lungs
97
clinical manifestations of tetralogy of fallot
```
severity directly related to pulmonic stenosis
becomes worse after DA closes
cyanosis, fatigue
hyper-cyanotic episodes
murmur
boot shaped heart on x-ray
```
98
what are triggers from hyper-cyanotic tet spells
crying, pooping, feeding, fever, dehydration
99
defect of transposition of great arteries
aorta & pulmonary artery are switched. 2 closed, non-communicating circuits
100
what are the two defects that are cyanotic?
tetralogy of fallot
| transposition of great arteries
101
clinical manifestations of transposition of great arteries
cyanosis at birth
hypoxemia with O2
progressive desaturation and acidosis
heart failure
102
what is heart failure
inability to heart maintain sufficient cardiac output to meet metabolic demands of tissues and organs
103
common causes for heart failure
myocardial ischemia
hypertension
cardiomyopathy
104
clinical manifestations of left sided heart failure
```
dyspnea
orthopnea (shortness of breath while lying down)
cough, crackles
hemoptysis
tachycardia
cool, pale skin
```
105
clinical manifestations of right sided heart failure
jugular vein distention
hepato-splenomegaly
weight gain, edema
106
treatment for congestive heart failure
manipulate preload, after load & contractility
improve cardiac output
minimize congestive symptoms
minimize cardiac workload
107
what is the most common complication of many congenital heart defects in pediatrics?
congestive heart failure
108
CHF in pediatrics is most often the result of what?
decreased left ventricular systolic function
109
treatment of CHF in pediatrics
```
treat underlying cardiac defect
fluid balance (increase calorie content of feedings, diuretics)
increase cardiac output
```
110
The 3 compensatory mechanisms that are triggered in heart failure work to restore cardiac output
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
Heart failure classifications - systolic
ventricles don't pump enough blood out
112
heart failure classifications - diastolic
ventricles don't fill properly
