Quiz2&Final Flashcards
1
Q
What do cells need for energy?
A
Glucose
2
Q
What hormone increases the amount of glucose in your blood?
A
glucagon
3
Q
What hormone decreases the amount of glucose in your blood?
A
Insulin
4
Q
Where is insulin produced?
A
Beta cells of pancreas
5
Q
When is the peak of Type 1 diabetes?
A
11-13 years old
6
Q
What ethnicity has a higher rate of type 1 diabetes?
A
Whites 1.5-2% higher
7
Q
What are the genetic percentages for type one diabetes?
A
Siblings: 5-`10%
Offspring: 2-5%
8
Q
What is the definition of type one diabetes?
A
It is absolute insulin insufficiency & an autoimmune attack on beta cells of pancreas
9
Q
What two components that go into type 1 diabetes?
A
Genetic components and environmental factors
10
Q
What is the pathophysiologic process of type 1 diabetes?
A
from the genetic components to the environmental factors–>autoantigenf form insulin-producing beta cells that circulate–>Activation of cellular and humoral immunity towards beta cells–>Destruction of beta cells=decreased insulin secretion
11
Q
In order to have signs and symptoms of type one diabetes, about what % of beta cells must die?
A
90%
12
Q
What are the 3 P’s of type 1 diabetes?
A
Polyuria- urination
Polydipsia- thirst
Polyphagia-hunger
13
Q
What are the signs &symptoms of type 1 diabetes?
A
weight loss 3 Ps weakness blurred vision nausea tingling in hands slow healing
14
Q
What is the most common treatment for type 1 diabetes?
A
Insulin therapy
15
Q
What are the evaluation methods for type 1 diabetes?
A
H&P
ketones/glucose in urine
Blood glucose
HgA1C levels
16
Q
What are the tests for blood glucose?
A
1-random sampling
2-fasting blood glucose
3-blood glucose concentrations
17
Q
What is the random sample level?
A
above 200 mg/dl
18
Q
What is the fasting blood glucose level?
A
Greater than 126mg/dl
19
Q
What is the blood glucose concentration levels?
A
Greater than 200 mg/dl 2 hrs after 75g oral glucose load.
**moms at 28 wks gestation
20
Q
What are the levels for HgA1C?
A
6.5 or higher
21
Q
What is the best evaluation test for type 1 diabetes and why?
A
HgA1C levels
because this shows how your body has done over the past few months
22
Q
What complications do you want to monitor in patients with type one diabetes?
A
Acute hyperglycemia
diabetic ketoacidosis
hypoglycemia
chronic changes
23
Q
What does TIRED stand for?
What are some other S&S?
A
S&S of hypoglycemia T- tachy I- irritable R- Restless E- Excessive hunger D- Diaphoresis/ Depression *Sweating, palor, hanger, lack of coordination
24
Q
What is the process that makes someone have ketoacidosis?
A
The adipose breaks down into ketones which are acidic
25
What is one of the most common reasons for a diabetic to be hospitalized?
Diabetic ketoacidosis
26
What are the causes of diabetic ketoacidosis?
being sick or stressed, infection or poor management of diabetes
27
What are the clinical symptoms of ketoacidosis?
low ph and low bicarb
tachypnea- fast and deep breaths calls kussmaul
fruity breath
hyperkalemia- the hydrogen/K buffer that exchanges
GI upset
hypotension
high blood sugar
28
What are the deep fast breaths that patients with diabetic ketoacidosis called?
Kussmaul
29
What does a patient with ketoacidosis need?
hydration
Insulin
Electrolyte replacement
30
What type of diabetes is most common?
Type 2
31
What race is most likely to have type 2 diabetes?
Non-caucasian
| Blacks& native americans
32
What is another group of people who are disproportionately affected by type 2 diabetes?
elderly
33
What are some risk factors of type 2 DM?
Obesity
Genetics
Metabolic syndrome
34
What is the definition of type two diabetes?
- Resistant to the action of insulin on peripheral tissues
| - The body has lost the ability to produce insulin
35
What are the two reasons why the body is resistant to insulin on the tissues?
the requirements for insulin have gone up
| & there is a lower glucose utilization
36
What are the two main components for why someone would get type 2 diabetes?
1- Genetic predisposition
| 2- Obesity- with diet and inactivity as components
37
While comparing type 1 & 2, what is different about the results of a urine test?
Type 1 will have glucose and ketones
| Type 2 will only have glucose
38
What is the treatment for type 2 diabetes?
**Lifestyle: diet, exercise, weight loss
| meds- oral and sometimes insulin(once pancreas is done)
39
What type of complications would you want to look for with type 2 diabetes?
chronic changes
40
What at the long term consequences of HYPERglycemia?
```
P.I.N.K.C.E.C
Peripheral vascular- feet problems
Infection- slow healing, gang green
Neuropathy
Kidneys- failure
Cardiovascular- failure, hypertension
Eyes- cataracts, diabetic retinopathy
Cerebrovascular- stroke
```
41
How much more insulin is needed while pregnant?
3x more than normal
42
What is the definition of gestational diabetes?
Glucose intolerance during pregancy
43
What are the two reasons that are thought to cause gestational diabetes?
placental hormones
weight gain
(bodies inability to make enough with increasing demands)
44
What are the risk factors for gestational diabetes?
Faily history, age, previous pregnancies with GD, large babies
45
At what time are pregnant mothers tested for gestational diabetes? With what test?
28 weeks
| glucose intolerance test
46
What is the treatment for gestational diabetes?
nutritional counseling and exercise
| *if not controlled then insulin may be used
47
What are complications of gestational diabetes?
baby 4g or more
hypoglycemia
still birth
48
What is something to be worried about when a mother has had gestational diabetes?
Developing DM within the next 10-20 years
| *routine screenings
49
What are glucocorticoids responsible for?
energy, immune response, inflammation and stress response
50
What are mineralocorticoids responsible for?
Na and fluid
| *primarily aldosterone
51
What are the two adrenocorticoid hormone disorders?
Addison's Disease
| Cushings Disease
52
What is primary adrenocorticoid insufficiency?
Addison's
| Caused by the destruction of adrenal cortex
53
What are the 3 components of Addison's?
Decreased secretions of
1) mineralocorticoids
2) Glucocorticoids
3) Androgens
54
What are the causes of Addison's Disease?
```
removal of adrenal gland
neoplasms
TB
autoimmune diseases
tumors
```
55
What is the most common cause of Addison's in developed countries?
Autoimmune
56
What are the clinical manifestations of Addison's?
- Decreased cortisol= low energy and hypoglycemia
- Deceased minerocorticoids= low BP, loss of Na and H2O
- Decreased androgens= body hair
- pigment changes
- GI disturbances
- Weight loss
57
What is the evaluation of Addison's?
history and a physical
labs- plasma cortisol levels
ACTH stimulation test= no/low rise in cortisol
Imaging- CT or MRI
58
What are the treatments of Addison's?
replacement hormones
| education on stress & dosing
59
What is Cushings Disease also called?
Hypercortisolism
60
What is the definition of Cushings?
cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids
61
What are the causes of cushings?
Pituitary hypersecretions of ACTH
Tumors
Administration of synthetic glucocorticoids or steroids
62
What are the clinical manifestations of Cushings?
```
Personality changes
Moon face
Fat deposits
Hyperglycemia
CNS irritability
Fluid retention
GI distress
Thin skin
Bruises, purple striae, petechiae
```
63
What is the evaluation for cushings?
History and physical
Labs- dexamethasone suppression test (high cortisol)
Imaging- ultrasound, CT/MRI,
64
What is the treatment for cushings?
surgery/radiation for tumors
| meds- antihypertensives, K, Diuretics
65
What is meningitis?
Inflammation and infection of the brain/spinal cord
66
What can cause meningitis?
bacteria, virus, fungi, parasites and toxins
67
What is the most common source of meningitis for peds?
Normal inhabitant that went to the wrong place
68
What are some other sources of meningitis?
blood stream, infection, trauma, fracture
69
What is the most common type of meningitis?
Bacterial
70
What are the 3 types of bacteria that cause meningitis and what ages do they affect the most?
pneumoniae- adults, 2nd for peds
Neisseria- Peds
E.Coli & group B strep- Newborns
71
What are the three steps to meningitis?
Invading organism
Inflammatory response
Cerebral Changes
72
Within the inflammatory response of meningitis, What actually happens?
neutrophils get clogged and exudate of CSF forms
| This causes a flow disruption of blood and leads to ischemia
73
The exudate that forms during meningitis causes the process to progress, how?
it continues the inflammatory response and includes more meningis = worse
74
What are the 3 categories of meningitis and clinical manifestations?
Infectious
Neurologic
Meningeal Irritation
75
What manifestations would infectious meningitis have?
fever
rash
chills
tachycardia
76
What manifestations would neurologic meningitis have?
```
Decreased LOC
Cranial nerve involvement
Seizures
Irritability
Delirium
```
77
What manifestations would meningeal irritation meningitis have?
throbbing headache
photophobia- light sensitivity
NUchal rigidity- limited neck movement
78
What are the two assessment tests for meningitis?
Kernig's sign
| Brudzinski's Sign
79
How would you test the Kernig's Sign?
flex hip 90* and try to extend knee- it will be painful
80
How would you test the Brudzinski's sign?
bend neck to chest- legs will flex in response due to pain
81
When taking a lumbar puncture for meningitis, What re the three things they are testing?
Culture and gram stains
Increased pressure
CSF testing
82
From the CSF test, what would tell someone has meningitis?
high WBC count
High neutrophils
High Protein
83
When someone has a bacterial meningitis, what would you see on a glucose screening?
Low glucose levels
84
When someone has a viral meningitis, what would you see from a glucose screening?
nothing- normal glucose readings would be found
85
What is the treatment for meningitis?
IV antibiotics - bacterial
Antiviral/ steroids- viral
Manage complications
Supportive care- rest, dark, low stimulation
86
How would you prevent meningitis?
Immunizations
Treatment of primary problems- infections
Sterile procedures
87
What should the normal ICP be?
0-15 mg Hg
88
What 3 things could cause ICP?
1-blood
2- brain matter
3- CSF
89
What are the 3 most common reasons for ICP?
Strokes (adults), trauma, tumors
90
What are the most common pediatric causes of ICP?
Tumor, structural malformations, infections
91
What are the 3 types of ICP?
Cerebral Edema
Space-occupying processes
Hydrocephalus
92
What happens with cerebral edema and cytotoxic edema?
causes ischemic tissue
damages ATP pumps
often occur together
93
What are 3 examples of space occupying processes?
tumors, hematomas, abscess
94
What is hydrocephalus?
An accumulation of CSF
95
What are some clinical manifestations of increases ICP?
headaches, LOC changes, pupil changes, vomiting, vital signs, seizures, decreased motor function. posturing
96
WHat types of Vital sign changes would happen with increased ICP?
increased SBP
Decreased pulse
Altered RR pattern
97
What are the clinical manifestations of increased ICP in and infant?
```
bulging fontanels
increases HC
HIgh pitched cry
poor feeding
sunsetting eyes
```
98
What is the treatment for ICP?
treat underlying cause
monitor, alleviate pressure (drain)
O2
Pharm
99
What is a seizure?
neurologic event with abnormal or excessive electrical discharges that can change motor function, sensation, autonomic visceral functions and behavior or consciousness
100
What are some reasons neonates would have seizures?
genetics, birth defects, infectons
101
The clinical manifestations of seizures depend on what 2 things?
What part of the brain it involved
| and where it spread to
102
What kind of things can trigger a seizure?
```
Stress
Lights
Stimuli
Infection
Fever
Lack of sleep
Constipation
head trauma
Drinking
```
103
What does epilepotogenic focus mean?
Where the seizure starts
104
What does prodromal/Aura mean?
having a subjective sense that seizure was going to happen
105
What does status epilepticus mean?
A seizure longer than 5 mins or back to back without recovery
106
What is a generalized seizure?
Involves entire brain
107
What is a Partial seizure?
involves part of brain surface
108
What does simple partial and complex partial mean?
simple- no impairment of consciousness
| Complex- impairment of consciousness
109
What is the biggest sign of a generalized seizure?
loss of consciousness
110
What does a absence or petite mal seizure mean?
staring
111
What is a myoclinic seizure?
a single , or several jerks
112
What is a atonic seizure?
drop attacks/ falling down
113
What is a tonic clonic seizure?
jerking of many muscles
114
What is the treatment for seizures?
```
Airway and safety
Document
treat cause
meds
avoid triggers
```
115
What are fibrile seizures?
Seizures accompanied by fever 100.4 or greater
| NO CNS involvement
116
What is cushings triad?
Increased Systolic BP
Decreased pulse
Altered Resperations
117
What is the pathophisiology behind having diabetic ketoacidosis?
Many times is triggered by being sick, stressed or having a infection and poor management of diabetes.
Results from increased breakdown of fats that are converted into ketones
118
What are AED drugs?
Antiepileptic drugs
119
What are the two groups of AEDs?
Traditional and Newer agents
120
There are 6 different drugs in this category, generally have more drug interactions, have more intense AE but cost less. What group is it?
Traditional
121
There are 13 different meds in this category and are generally very expensive. What category?
Newer
122
This group of drugs are more tolerable and are safer during pregnancy .
Newer
123
What category of drugs should be avoided during pregnancy?
Traditional AEDs
124
What are the three most commonly used traditional drugs?
Phenytoin
Valproic Acid
Carbamazepine
125
What is the one type of seizure that phenytoin does not work for?
Absence seizures
126
How does phenytoin work?
Selective inhibition of sodium channels to prevent the entrance of sodium into hyperactive neurons
127
What is the half-life of phenytoin?
Depends on the does- smaller doses have smaller half life
128
Where is phenytoin metabolized?
in the liver- metabolism i limited
129
What is a normal loading dose of phenytoin? What route would be used?
15-20 mg/kg
IV - used while having a seizure or in coma
or PO
130
What are the maintenance doses of phenytoin?
| What is the theraputic range? toxic?
Determined by plasma concentrations
10-20 mcg/mL
over 20 is toxic
131
What are the signs an symptoms of phenytoin toxicity?
Nystagmus, sedation, ataxia, diplopia, seizures
132
T/F
| Phenytoin has a lot of adverse effects?
TRUE- it is a traditional AED and has many
133
What are the AE of phenytoin?
Gingivial hyperplasia : swelling tender and bleeding
Dermatologic effects- rash, measles-like- purple glove syndrome
Teratogenic outcomes- Cleft palate, hydrocephalus, renal defects, micromedlia, decreased vit K clotting factors
134
When phenytoin is given IV, what are some things to consider?
Cardiovascular effects- dysrhythmia, hypotension
| INFUSE SLOWLY
135
What is the best way to administer phenytoin?
IV central access
136
What is fosphenytoin?
| how is it administered?
It is converted into phenytoin in the body
| ONLY IV
137
What are the benefits of using fosphenytoin vs. phenytoin?
It is easier to administer
less AE- does not cause purple glove
Can be infused faster
138
How much faster can fosphenytoin be infused?
3x faster
139
When giving fosphenytoin, even though it can be infused faster, it won't work as fast- Why?
Needs to be converted before it can be utilized.
140
What is the biggest problem with phenytoin?
drug interactions
141
What types of seizures is carbamazepine used for?
partial and tonic-clonic
142
How does carbamazapine work in the body?
suppresses high-frequency neuronal discharge at foci
143
What are some interesting pharmacokinetics about carbamazeoine?
* metabolism
* loading dose
It is metabolized by liver b/c autoinduction
Half life decreases with continued therapy
No loading dose possible- slow increases needed
144
What are some AE of carbamazepine?
CNS - vision, dizziness (falls) **can build tolerance
Hematologic- bone marrow suppression (MONITOR)
TERATOGEN - spina bifida
Hyponatremia - Altered mental status/ unsteady
Dermatologic- rash, photosensitivity*
145
Why is valproic acid a bad option for people to take?
The frequency is too high 4x/dy
146
What are the three potential* MOA of divalproex?
sodium channel blockage
calcium channel suppression
inhibits GABA
147
What are the AE of divalproex?
N/V
Hepatoxicity- not in children under 2*** can be fatal
Hyperammonemia
Teratogenic- in 1st tri especially - congenital malformations 4x higher than other AEDs- neural tube defects, impaired cog
148
What are the drug interactions like with divalproex?
Complex- and have a synergistic effect with phenobarbital and phenytoin
149
Why is Levetricetam such a good option?
- used for many type of seizures
- minimal drug interactions
- mild to moderate side effects
- IV or PO
150
What is one of the most important things to remember when administering mannitol IV??
FILTERED TUBING
| inspect- can crystalize
151
What are some AE of mannitol?
Dehydration
decreased BP
decreased electrolytes
Serum osmolarity
152
Mannitol is good for cerebral edma and getting fuild off the brain, why?
it is an osmotic diuretic
153
What is the leading case of acute and chronic illness in children and the most frequent admitting diagnosis?
Asthma
154
What are the 3 characteristic mechanisms of obstructive airway disease?
Bronchospasms
Inflammation and edema
reactivity to a variety of stimulli
155
What are the high risk pops for asthma?
African american and hispanics
pops in inner-city
premature- low birth weights
156
When does intrinsic asthma have its onset?
adult onset
| with no history
157
When does extrinsic asthma have its onset?
in childhood
158
What is status asthmaticus?
Can't get the asthma attack to stop
159
What are the two responses of Asthma?
Early- inflammation
| Late- 4-8 hrs later
160
What is the pathophisiology of the early response of asthma?
Allergen binds to mast cell
mast cells degranulate and mediators are released (histamine)
Vasodilation and increased acetylcholine
161
What causes the direct tissue damage in the late response of asthma?
eosinophils
162
What is airway remodeling?
when there is chronic inflammation in the airway, the tissues are actually changed
163
What three things happen with airway remodeling?
Basement membrane becomes thick
Mucous glads increase in numbers
Smooth muscles hypertrophy
164
What are some severe clinical manifestations of asthma?
```
cynosis
retractions, nasal flaring
decreased breath sounds
agitation
can't speak well
Decreased systolic pressure during inspiration
```
165
What are the treatments for asthma?
manage allergens
peak flow meters
meds
166
What is bronchiolitis?
inflammation of the brochioles- secondary to infection normally
Seasonal
Lower airway
167
What is the pathophisiology behind bronchiolitis?
fibrin plugs
air trapping- hyperinflation
increased work of breathing
168
What are the clinical manifestations of bronchiolitis?
```
Rhinorrhea and tight cough
decreased appetite, lethergy, fever
tachypnea- retractions
abnormal sounds
hyperexpanded
```
169
What is the treatment for bronchiolitis?
supp O2
increased hydration
inhaled hypertonic saline
NG tube feeds
170
Virchow's triad
Vessel wall injury
circulatory stasis
hypercoagulable conditions
171
What are the two first clinical manifestations you will see when someone has a pulmonary embolism?
DYSPNEA
| restlessness, apprehension and anxiety
172
What are two short acting inhaled bronchiodilators?
Albuterol and Ipratropium
173
Which type of inhalation med has less systemic side effects?
DPI- dry powder
174
corticosteriods will help decrease what?
```
Inflammatory cells and Structural cells**
cytokines
mast cell numbers
macrophage numbers
mucus secretions
```
175
beclomethosone
Inhaled corticosteroid
minimal systemic absorption
can be MDI
176
What are the most common AE of beclomethasone?
Oral candidiasis
Dysphonia- crackle talk
promotes bone loss
**rinse mouth**
177
Albuterol
inhaled brochodilator
Beta- agonist
short acting- used for exercise induced
Immediate use-last 30 to 60 mins
178
Ipratropium
Inhaled bronchodilator
Anticholingerics- blocks muscarinic receptors
short actingmay last for 6 hrs
179
What are the AE of albuterol?
tachycardia, tremor, hypokalemia
180
What are the AE of Ipratropium?
minimal systemic
dry mouth
pharyngeal irritation
181
Montelukast
*controller med
supresses leukotrines
Oral BID- or 2 hrs before workout
182
What are the 4 broad types of genetic disorders?
Chromosomal anomalies- number and structure
Single-Gene disorder- dom/rec.x-link
Polygenic/multifactoral
Other
183
What is it called when someone has anything other than 46 chromosomes?
aneuploidy
184
Between a sex linked anomaly and a monosomy, which is more dangerous and debilitating?
Sex inked is more common and less troubling but monosomy is more problematic
185
What are the 5 types of abnormal structures?
```
Deletion
Duplicates
Inversions
Insertion
Translocations
```
186
What is translocation?
One part of chain is flipped
187
What is a point mutation?
Substitution of a single base pair and either does/doesn't change amino acid
188
What is a frameshift mutation?
addition or deletion of 1 or 2 nucleotides
| * changes all codons after the shift
189
Autosomal Recessive Disorder
AA-none
Aa-carrier
aa- affected
**unaffected can still pass if they carry
190
Autosomal Dominant Disorder
AA- Affected
Aa- Affected
aa-none
**unaffected do not pass it
191
What is an example of autosomal dominant disorder?
huntingtons disease
192
What is another name for AA?
Aa?
aa?
Homozygous Dominant
Heterozygous
Homozygous Recessive
193
What gender sees x-linked recessive more?
males
194
What are 2 examples of x-linked recessive ?
Hemophilia A
| Duchenne Muscular Dystrophy
195
What are polygenic traits?
traits that are a result of several genes acting together
196
What are multifactorial ?
Genes thar makes someone susceptible
197
What is penetrance?
phenotype associated with genotype
| ** reason why it may skip generations
198
What is expressivity?
Extent of variation- environmental factors and other genes
199
Down Syndrome
trisomy 21
nondisjunction
translocation
mosaicism
200
Duchenne muscular dystrophy ?
```
only males
by age 3
deficient in protein
leaks creatinine
necrosis/degeneration
gradual loss
```
201
Sickle cell affects which chromosome?
11- point mutation
202
What are some triggers for sickle cell crises?
Dehydration, cold, infection, hypoxia, fever, acidosis
203
What are the two parts of sickle cell anemia?
Sickling- occlusion-stickin, pain, tissue damage
| Anemia- short lifespan, hyperbilirubinemia
204
What are the two inflammatory bowel diseases?
Ulcerative colitis and chron's disease
205
What is the definition of ulcerative colitis?
inflammatory disease of the mucosa of the colon and rectum
206
When ifs the onset of the inflammatory bowel diseases?
childhood and young adulthood
207
Chrons disease affects what part of the GI?
Mouth to anus, has skip lesions so it may affect a different part with exacerbations
208
UC affects what part of the GI?
Large intestines, continuous
209
Which inflammatory disease has a cobble stone apperance and why?
Crohns disease has a cobble stone appearance because of the granulomas
210
What are some of the factors for inflammatory diseases?
jewish decent, family history, white, immunological factors, environmental factors
211
What starts the process of UC in the GI system?
| How does it continue?
1-Inflammation at base of crypts- activated neutrophils and macrophages
2-abscess formation
3-abscessess come together and form ulcers
4-repair- fragile
212
What are some clinical manifestations of UC?
diarrhea because of a lack of ability to absorb water
rectal bleeding
pain in abdomen
213
How would UC be diagnosed?
Hx-P
| Biopsy- ulcers
214
What is used to treat UC?
corticosteroids
immunosuppresants
nutritional management
antibiotics
215
What types of nutritional changes would someone with UC have to incorporate?
no milk, low fiber, low fat, increase protein
216
What part of the GI system does Chrons affect?
Mouth the anus, but there are skip lesions, so not all will be affected at once
217
What is the cardinal feature of Chrons?
Granulomas
218
What starts the exacerbation of Chrons?
1-blockage of the GI lymphoid and lymphatic structures
2-Engorged//inflammed= deep ulcers
3-tickened by fibrous scor, deep fistulas-openings
219
What are the clinical manifestations of Chrons?
incapable of adequately absorbing nutrients -weight loss, malnutrition, hight/wt
- skipping lesions
- perianal fissures, fistulas and abscesses
220
In what situation would someone with inflammatory bowel need to get a colectomy?
if there was high grade dysplasia
221
What type of inflammatory bowel would the following person have?
Severe abdominal pain, occasional diarrhea with no blood and is very thin and continues to have weight loss?
Chron's Disease
222
When someone tells you they have bloody stools an diarrhea on many occasions, what type of inflammatory bowel would you think they have?
Ulcerative colitis
223
Malabsorption is more common with with IBD?
Chron's Disease
224
What age group is GERD most likely to affect?
0-6 moths and adults
225
What is the definition of GERD?
backflow of gastric contents into the esophagus through the lower esophageal sphincter (LES)
226
What are the three broad causes of GERD?
1- issues with LES- strength and efficacy
2- increases in intraabdominal pressure
3- delayed gastric emptying
227
What are some examples/reasons of GERD as a result of LES issues?
high fat diet, caffeine, alcohol, smoking, obesity and meds
228
What are some examples/reasons of GERD as a result of intraabdominal pressure?
pregnancy, constipation, tumor, overfeeding, crying
229
What are some examples/reasons of GERD as a result of delayed gastric emptying?
being an infant
230
What are some clinical manifestations of GERD?
heartburn, regurgitation, chest pain, dysphasia.
| infants often will not have symptoms- physiologic reflex
231
What are two complications of GERD?
1-aspiration- asthma, coughing, laryngitis
| 2- highly acidic in esophagus - structures, narrowing
232
What is some treatment for GERD?
diet/behavior- low fat diet, low caffeine, and no smoking
Antacids and histamine blockers
proton pump inhibitors.
233
What are some treatment options for infants with GERD?
small frequent meals and burping
thickened feeding controversial
positioning
meds
234
What are some common presenting symptoms of GERD in infant patients?
```
feeding refusal,
recurrent vomiting
irritability
poor weight gain
sleep problems
resp symptoms
```
235
What are some common presenting symptoms of GERD in older children or adolescent patients?
```
abd pain and heartburn
vomiting
dysphagia
asthma
pneumonia
upper airway symptoms
```
236
What is osteomyelitis?
Severe infection of bone and local tissue
237
What are the two most common organisms of osteomyelitis?
staph aureus
| strep pneumaniae
238
what are the three ways osteomyelitis can reach the blood?
bloodstream
adjacent soft tissue injury
direct introduction of organism into the bone
239
Who are people at high risk for osteomyelitis?
those who have had surgery- contamination
open fractures
IV drug users
kids less than 16 and older adults
240
What is the treatment for osteomyelitis?
4-6 weeks of IV antibiotics OR IV to oral
debridement if needed
removal of prosthesis or other materials
241
How would osteomyelitis be diagnosed?
X-ray,
increased WBC, CRP, ESR- inflammation and infection
bone scan
blood cultures and bone aspirate
242
What are the differences in pediatric bones?
less brittle, higher collagen to bone ratio
Stronger periosteum
Presence of epiphyseal plate
243
What would you expect the X-ray of a comminuted bone fracture to look like?
Fragments of broken bones
244
What is an epiphyseal fracture?
a break through the growth plate of a bone
245
What is the process of healing of a cortical bone?
```
Bleeding
Hematoma
Osteoblasts and calcium
Callus formation
Callus reabsorbed
```
246
What are the assessments for compartment syndrome ?
```
5 Ps
pain
paralysis
parasthesis
pallor
pulses
```
247
What are some complications of a fracture?
```
delayed healing
compartment syndrome
fat embolism syndrome
osteonecrosis
osteomyelitis
DVT
neurovascular injury
```
248
What is Ranitidine also known as?
Zantac
249
What is Zantac used for?
It is a histamine2 receptor antagonist
Oral and IV
OTC and Rx
250
What are two things users of Zantac should know?
*Caution in pregnancy*
| Drug interactions!
251
What is Omeprozole also known as?
Prilosec
252
What does Omeprozole do in the body?
irreversible Inhibits the proton pump
blocks gastrin production
*PO or IV
OTC or Rx
253
What is a long-term effect of Omeprozole?
increases risk of osteoporosis= increased fracture risk- decreased absorption of calcium
254
What are some increased risks when taking omeprozole?
Pneumonia
C-diff
Dementia
Kidney injury
255
Surcralfate is what type of drug?
Mucosal protectant
256
How does Sucralfate work?
Adheres to ulcer for up to 6 hours to protect and prevent more damage
257
What are some AE of Sucralfate?
constipation
can decrease absorption of other meds
*caution in pregnancy
258
Milk of Magnesia is also called ____?
magnesium hydroxide
259
What is the proper name for tums?
calcium carbonate
260
MOM and tums are used for what?
neutralize gastric acid and inactivate pepsin
| *potential mucosal protectant
261
What are the AE of Antacids?
constipation and diarrhea
262
What should people taking antacids be aware of?
* caution in pregnancy
* avoid with GI perforation or obstruction
* caution with renal dysfunction
263
What are some ways to treat IBD?
```
5-aminosalicylates
Glucocorticoids
Immunosuppressants
Immunomodulators
Antibiotics
```
264
What are the mild treatment options for UC according to the pyramid?
Topical or oral aminosalicylates
| Probiotics
265
What are the moderate treatment options for UC according to the pyramid?
immunomodulators
corticosteroids
Infliximab
266
What are the severe treatment options for UC according to the pyramid?
```
Colectomy
Inflixamab
Antibodies
cyclosporine
Experimental Rx
```
267
What are the mild treatment options for Chron's according to the pyramid?
Antibiotics
Aminosalicytates
budesonide
fish oil- probiotics
268
What are the moderate treatment options for Chron's according to the pyramid?
Inflixamab
Immunomodulators
corticosteroids
methotrexate
269
What are the Severe treatment options for Chron's according to the pyramid?
Surgery
Adalimemab
clinical trials
270
Sulfasalazine is what type of drug and how does it work?
5-aminosalicylate
| Decreases inflammation by inhibiting prostaglandin synthesis
271
What are some AE of Sulfaslazine ?
Blood disorders and anemia
272
where is sulfasalazine metabilized?
in the intestinal flora
273
How is sulfasalazine administered?
Oral or Rectal-enema or suppository
274
What are 5 types of drugs most commonly used for mental health?
1- Selective Seratonin Reuptake Inhibitors SSRIs
2- Tricyclic Antidepressants TCAs
3- Serotonin-Norepinephrine Reuptake Inhibitors
4- Atypical Antidepressants
5- Benzodiazapines
275
What is an example of an SSRI?
Paroxetine- Paxil
276
What is an example of a TCA?
Nortriptyline
277
What is an example of Serotonin-norepinephrine reuptake inhibitor?
Venlafaxine- Effexor
278
What is an example of atypical antidepressant?
Bupropoin- Wellbutrin
279
What is an example of a benzodiazapine?
Alprazolam- Xanax
280
When taking Paroxetine, what are some things you should know?
*drug interactions
*may take 4-8 weeks to have an effect
Could have the following AE
sexual dysfunction
weight gain
withdrawal syndrome
Serotonin syndrome
281
What would be some indicators that you have serotonin syndrome?
muscle rigidity
fever
altered mental syndrome
282
When taking SSRIs, what other drugs should you be aware of?
Anything that has an antiplatelet agent
283
What type of mental health drugs are fairly dangerous and have lethal toxicity problems?
TCAs
284
What is an example of a TCA?
Amitriptyline
285
What is Amitriptyline most commonly used for?
Sleep and neuropathic pain
| *not for depression
286
How does Amitriptyline work?
blocks neuronal reuptake of NE and serotonin
287
What are the significant side effects of Amitriptyline?
```
Orthostatic hypotension
sedation
anticholinergic effects
cardiac toxicity
Seizures
```
288
What is an example of serotonin-norepinephrine reuptake inhibitor?
Venlafaxine
289
How does Venlafaxine work?
Blocks the reuptake of NE and serotonin- Similar to SSRIs
290
What are the adverse effects of Venlafaxine?
Weight gain, HA, insomnia, dizziness, sexual dysfunction, serotonin syndrome, hypertension and tachycardia
291
What two types of drugs should somene taking serotonin-norepinephrine reuptake inhibitor be careful of taking together?
NSAIDs and anticoagulants
292
What is an example of a drug used for atypical antidepression and what is it used for?
Bupropion
| used for smoking
293
What are some adverse effects of Bupropion?
```
agitation
HA, dry mouth
constipation
weight loss
Serious= Seizures
```
294
How many types of formulations does Bupropion have?
3
immediate
sustained
XL tabs
295
How long will it take for a response to antidepressants?
weeks
| *max response at 3 months
296
What is the MOA of benzodiazapines?
intensifies GABA
297
What are the effects of Benzos?
reduced anxiety
promotes sleep
muscles relaxant
**can have withdrawal symptoms
298
What is an example of a benzodiazapine?
Alprazolam
| aka Xanax
299
What are the AE of Xanax?
CNS depression
Respiratory depression
Anterograde amnesia
300
What is the goal of medical treatment for heart failure?
To prevent and decrease damage to heart
301
What is the last line of medication used for heart failure?
inotropic support which improves contractility
302
What two types of drugs have damaging effects on the myocardium?
Catecholamines and angiotensin 2
303
What type of diuretics would you use if you wanted a big effect?
Loop diuretics
304
When taking a diuretic for symptom management, what type would you take?
Loop diuretics
305
What is an example of a loop diuretic?
furosemide aka lasiks
306
What is the biggest AE to be aware of when taking furosemide?
hypokalemia
| also, hypotension
307
What two types of diuretics are commonly used together and why?
loop diuretics and potassium sparing diuretics
because loop diuretics can cause hypokalemia, it is smart to use a potassium sparing diuretic because it will help prevent this
308
What is an example of a potassium sparing diuretic?
spironolactone
| for mild diuresis
309
What is an example of thiazide diuretics?
Hydrochlorothiazide
310
What are the AE of hydrochlorothiazide?
hypokalemia and hypertension
311
What are the AE of spironolactone?
hyperkalemia and gynecomasita in men
312
If a patient has poor GFR, which type of diuretic do you know will still work?
loop diuretics
313
What is an example of an ACE inhibitor?
lisinopril
314
By blocking the ACE, what are you doing and preventing overall?
Decreasing mortality, improving function and preventing remodeling= angio1--angio2--vasoconstriction to remodeling
315
What are the AE of lisinopril?
angioedema, cough and hyperkalemia
316
What is an example of an angiotensin II receptor blocker?
losartin
317
What are the AE of losartin?
hyperkalemia and less angioedema
318
What are the beniftis of taking an angiotensin II receptor blocker?
```
improve LV EF
reduce symptoms
increase exercise tolerance
decrease hospitalizations
enhance QOL
reduce mortality
```
319
If someone were to have severe heart failure, which drug would be best?
Losartin
320
Why would you not want to give someone with hear failure amlodapine?
Causes peripheral edema and you don't want edema with heart failure patients
321
What type of drug would you want to use, add, later own the heart failure road?
aldosterone antagonist- spironolactone
322
Beta blockers can do what 5 things?
```
improve LVEF
increase exercise tolerance
Slow progression of HF
Reduce need for hospitalization
Prolong survival
```
323
What is an example of a cardiac glycoside?
Digoxin
324
What is the biggest effect that digoxin has that can also cause many of the AE?
Inhibits Na-K- ATPase pump=hypokalemia, hyperkalemia
| heart dysrhythmias
325
What are some AE of digoxin?
```
Heart dysrhythmias
anorexia
nausea
vomting
halo- visual disturbances
```
**many drug interactions**
326
What is an example of a vasodilator?
Hydralazine
327
What does hydralazine do?
selective dilation of arterioles
*combo with nitrates
328
NItroglycerin is commonly used for what?
chest pain- dilates veins and decreases venous return and decreases O2 demands
329
Why have there been deaths from nitro?
drastic drop in BP
330
What is the foramen ovale?
the whole between the R atrium and L atrium- closes after birth
331
What is the ductus arteriosus?
The the shunt from the pulmonary artery to the aorta- bypass the lungs
332
What are some environmental reasons someone would get a congenital heart disease?
```
infections
metabolic disease
drug exposure
alcohol
increase maternal age
```
333
What are the two ways CHD is classified?
Cyanotic and Acyanotic
- Blood flow to lungs
- obstruction
- mixed blood
334
What CHD are acyanotic and have increased pulmonary bloodflow?
PDA, ASD & VSD
335
What CHD is an obstruction?
coarctation of the aorta
336
What CHD had a decrease in pulmonary blood flow?
Teralogy of Fallot
337
What CHD has mixed blood flow?
Transposition of the great arteries
338
What side of the heart has a greater pressure gradient ?
left
339
If the heart is having to work harder than normal What will happen to the muscle?
hypertrophy
340
What is PDA?
Patent ductus arteriosus
hole between the pulmonary artery and aorta
** normally closes within 24-72 hrs of birth
blood goes back into the pulm. artery after being oxygenated
341
Where is the workload going to in PDA?
workload to the lungs= pulmonary hyepertension and right sided heart failure
342
What med is given to close the opening from PDA?
Indomethacin
343
What are some clinical manifestations of PDA?
murmur
widened pulse pressure
bounding pulses
344
What is ASD?
opening in the septum between the aorta and right atrium -foramen ovale
345
whre is the workload in ASD?
right sided with right sided failure
346
Where is the pressure in the heart with ASD?
in the right. Blood moves from aorta to right atrium
347
What are some clinical manifestations of ASD?
fatigue, dyspnea with exertion, resp infections, murmur
348
What is coarctation of the aorta?
Narrowing of the aorta
| *most common around ductus arteriosus
349
Where is the workload with Coarctation?
left sided-with hyertrophy
| *pulmonary manifestatins
350
What are some clinical manifestations with coarctation of aorta?
murmur
poor lower extremity perfusion
pulse and BP differences in upper and lower
Initial L sided heart failure
351
What drug is given to keep ductus arteriosus open?
prostaglandin E
352
What 4 things are wrong with tetralogy of fallot?
VSD
Overriding aorta- crossover to both ventricles
Pulmonary stenosis
RV hypertrophy
353
Where is the workflow in Tetralogy?
Right sided --> pulmonary stenosis
354
What are some clinical manifestation of Tetralogy?
Cyanosis, fatigue
murmur
tet spells
boot shaped heart on XRAY
355
What is a tet spell and what happens?
normally will happen when people eat, cry, poop= more unoxygenated blood out to the body= blue
356
What is transposition of the great arteries?
The aorta and pulmonary artery are switched
| **not compatable with life
357
Pathologically, what is happening to the blood with transposition?
The RV is sending unoxygenated blood to the body
| The LV is sending oxygenated blood to thr lungs
358
What three things do you want to control when managing CHF?
Stroke volume
- Preload
- contractility
- afterload
- heart rate
359
What is happening with systolic heart failure?
ventricles don't pump enough blood out
| low EF
360
What is happening with diastolic heart failure?
Ventricles don't fill properly
361
What are clinical manifestations of left sided heart failure?
```
Dyspnea, orthopnea
cough
crackles
hemoptysis
Tachy
cool, pale
```
362
What are clinical manifestations of right sided heart failure?
Jugular vein distestion
Hepato-splenomegaly
Weight gain, edema
363
What drug helps improve cardiac output?
digoxin
364
What type of drugs help minimize congestive symptoms ?
diuretics
365
With depression, Where is pharm most focused?
within the deficiency of monoamines
366
What is the monoamine deficiency theory?
```
Not as much in synaptic space
1- decrease in baseline neurotransmitters
2- overactive reuptake
3- Enzymes
4- Transporters are low
```
