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Pharm/Patho > Quiz2&Final > Flashcards

Quiz2&Final Flashcards

1
Q

What do cells need for energy?

A

Glucose

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2
Q

What hormone increases the amount of glucose in your blood?

A

glucagon

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3
Q

What hormone decreases the amount of glucose in your blood?

A

Insulin

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4
Q

Where is insulin produced?

A

Beta cells of pancreas

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5
Q

When is the peak of Type 1 diabetes?

A

11-13 years old

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6
Q

What ethnicity has a higher rate of type 1 diabetes?

A

Whites 1.5-2% higher

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7
Q

What are the genetic percentages for type one diabetes?

A

Siblings: 5-`10%
Offspring: 2-5%

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8
Q

What is the definition of type one diabetes?

A

It is absolute insulin insufficiency & an autoimmune attack on beta cells of pancreas

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9
Q

What two components that go into type 1 diabetes?

A

Genetic components and environmental factors

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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

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11
Q

In order to have signs and symptoms of type one diabetes, about what % of beta cells must die?

A

90%

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12
Q

What are the 3 P’s of type 1 diabetes?

A

Polyuria- urination
Polydipsia- thirst
Polyphagia-hunger

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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
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14
Q

What is the most common treatment for type 1 diabetes?

A

Insulin therapy

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15
Q

What are the evaluation methods for type 1 diabetes?

A

H&P
ketones/glucose in urine
Blood glucose
HgA1C levels

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16
Q

What are the tests for blood glucose?

A

1-random sampling
2-fasting blood glucose
3-blood glucose concentrations

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17
Q

What is the random sample level?

A

above 200 mg/dl

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18
Q

What is the fasting blood glucose level?

A

Greater than 126mg/dl

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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

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20
Q

What are the levels for HgA1C?

A

6.5 or higher

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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

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22
Q

What complications do you want to monitor in patients with type one diabetes?

A

Acute hyperglycemia
diabetic ketoacidosis
hypoglycemia
chronic changes

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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
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24
Q

What is the process that makes someone have ketoacidosis?

A

The adipose breaks down into ketones which are acidic

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25
Q

What is one of the most common reasons for a diabetic to be hospitalized?

A

Diabetic ketoacidosis

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26
Q

What are the causes of diabetic ketoacidosis?

A

being sick or stressed, infection or poor management of diabetes

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27
Q

What are the clinical symptoms of ketoacidosis?

A

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

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28
Q

What are the deep fast breaths that patients with diabetic ketoacidosis called?

A

Kussmaul

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29
Q

What does a patient with ketoacidosis need?

A

hydration
Insulin
Electrolyte replacement

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30
Q

What type of diabetes is most common?

A

Type 2

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31
Q

What race is most likely to have type 2 diabetes?

A

Non-caucasian

Blacks& native americans

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32
Q

What is another group of people who are disproportionately affected by type 2 diabetes?

A

elderly

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33
Q

What are some risk factors of type 2 DM?

A

Obesity
Genetics
Metabolic syndrome

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34
Q

What is the definition of type two diabetes?

A
  • Resistant to the action of insulin on peripheral tissues

- The body has lost the ability to produce insulin

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35
Q

What are the two reasons why the body is resistant to insulin on the tissues?

A

the requirements for insulin have gone up

& there is a lower glucose utilization

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36
Q

What are the two main components for why someone would get type 2 diabetes?

A

1- Genetic predisposition

2- Obesity- with diet and inactivity as components

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37
Q

While comparing type 1 & 2, what is different about the results of a urine test?

A

Type 1 will have glucose and ketones

Type 2 will only have glucose

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38
Q

What is the treatment for type 2 diabetes?

A

**Lifestyle: diet, exercise, weight loss

meds- oral and sometimes insulin(once pancreas is done)

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39
Q

What type of complications would you want to look for with type 2 diabetes?

A

chronic changes

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40
Q

What at the long term consequences of HYPERglycemia?

A 
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
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41
Q

How much more insulin is needed while pregnant?

A

3x more than normal

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42
Q

What is the definition of gestational diabetes?

A

Glucose intolerance during pregancy

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43
Q

What are the two reasons that are thought to cause gestational diabetes?

A

placental hormones
weight gain
(bodies inability to make enough with increasing demands)

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44
Q

What are the risk factors for gestational diabetes?

A

Faily history, age, previous pregnancies with GD, large babies

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45
Q

At what time are pregnant mothers tested for gestational diabetes? With what test?

A

28 weeks

glucose intolerance test

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46
Q

What is the treatment for gestational diabetes?

A

nutritional counseling and exercise

*if not controlled then insulin may be used

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47
Q

What are complications of gestational diabetes?

A

baby 4g or more
hypoglycemia
still birth

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48
Q

What is something to be worried about when a mother has had gestational diabetes?

A

Developing DM within the next 10-20 years

*routine screenings

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49
Q

What are glucocorticoids responsible for?

A

energy, immune response, inflammation and stress response

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50
Q

What are mineralocorticoids responsible for?

A

Na and fluid

*primarily aldosterone

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51
Q

What are the two adrenocorticoid hormone disorders?

A

Addison’s Disease

Cushings Disease

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52
Q

What is primary adrenocorticoid insufficiency?

A

Addison’s

Caused by the destruction of adrenal cortex

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53
Q

What are the 3 components of Addison’s?

A

Decreased secretions of

1) mineralocorticoids
2) Glucocorticoids
3) Androgens

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54
Q

What are the causes of Addison’s Disease?

A 
removal of adrenal gland
neoplasms
TB
autoimmune diseases
tumors
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55
Q

What is the most common cause of Addison’s in developed countries?

A

Autoimmune

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56
Q

What are the clinical manifestations of Addison’s?

A
  • 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
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57
Q

What is the evaluation of Addison’s?

A

history and a physical
labs- plasma cortisol levels
ACTH stimulation test= no/low rise in cortisol
Imaging- CT or MRI

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58
Q

What are the treatments of Addison’s?

A

replacement hormones

education on stress & dosing

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59
Q

What is Cushings Disease also called?

A

Hypercortisolism

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60
Q

What is the definition of Cushings?

A

cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids

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61
Q

What are the causes of cushings?

A

Pituitary hypersecretions of ACTH
Tumors
Administration of synthetic glucocorticoids or steroids

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62
Q

What are the clinical manifestations of Cushings?

A 
Personality changes
Moon face
Fat deposits 
Hyperglycemia
CNS irritability
Fluid retention
GI distress
Thin skin
Bruises, purple striae, petechiae
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63
Q

What is the evaluation for cushings?

A

History and physical
Labs- dexamethasone suppression test (high cortisol)
Imaging- ultrasound, CT/MRI,

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64
Q

What is the treatment for cushings?

A

surgery/radiation for tumors

meds- antihypertensives, K, Diuretics

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65
Q

What is meningitis?

A

Inflammation and infection of the brain/spinal cord

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66
Q

What can cause meningitis?

A

bacteria, virus, fungi, parasites and toxins

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67
Q

What is the most common source of meningitis for peds?

A

Normal inhabitant that went to the wrong place

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68
Q

What are some other sources of meningitis?

A

blood stream, infection, trauma, fracture

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69
Q

What is the most common type of meningitis?

A

Bacterial

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70
Q

What are the 3 types of bacteria that cause meningitis and what ages do they affect the most?

A

pneumoniae- adults, 2nd for peds
Neisseria- Peds
E.Coli & group B strep- Newborns

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71
Q

What are the three steps to meningitis?

A

Invading organism
Inflammatory response
Cerebral Changes

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72
Q

Within the inflammatory response of meningitis, What actually happens?

A

neutrophils get clogged and exudate of CSF forms

This causes a flow disruption of blood and leads to ischemia

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73
Q

The exudate that forms during meningitis causes the process to progress, how?

A

it continues the inflammatory response and includes more meningis = worse

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74
Q

What are the 3 categories of meningitis and clinical manifestations?

A

Infectious
Neurologic
Meningeal Irritation

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75
Q

What manifestations would infectious meningitis have?

A

fever
rash
chills
tachycardia

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76
Q

What manifestations would neurologic meningitis have?

A 
Decreased LOC
Cranial nerve involvement 
Seizures 
Irritability
Delirium
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77
Q

What manifestations would meningeal irritation meningitis have?

A

throbbing headache
photophobia- light sensitivity
NUchal rigidity- limited neck movement

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78
Q

What are the two assessment tests for meningitis?

A

Kernig’s sign

Brudzinski’s Sign

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79
Q

How would you test the Kernig’s Sign?

A

flex hip 90* and try to extend knee- it will be painful

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80
Q

How would you test the Brudzinski’s sign?

A

bend neck to chest- legs will flex in response due to pain

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81
Q

When taking a lumbar puncture for meningitis, What re the three things they are testing?

A

Culture and gram stains
Increased pressure
CSF testing

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82
Q

From the CSF test, what would tell someone has meningitis?

A

high WBC count
High neutrophils
High Protein

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83
Q

When someone has a bacterial meningitis, what would you see on a glucose screening?

A

Low glucose levels

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84
Q

When someone has a viral meningitis, what would you see from a glucose screening?

A

nothing- normal glucose readings would be found

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85
Q

What is the treatment for meningitis?

A

IV antibiotics - bacterial
Antiviral/ steroids- viral
Manage complications
Supportive care- rest, dark, low stimulation

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86
Q

How would you prevent meningitis?

A

Immunizations
Treatment of primary problems- infections
Sterile procedures

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87
Q

What should the normal ICP be?

A

0-15 mg Hg

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88
Q

What 3 things could cause ICP?

A

1-blood
2- brain matter
3- CSF

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89
Q

What are the 3 most common reasons for ICP?

A

Strokes (adults), trauma, tumors

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90
Q

What are the most common pediatric causes of ICP?

A

Tumor, structural malformations, infections

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91
Q

What are the 3 types of ICP?

A

Cerebral Edema
Space-occupying processes
Hydrocephalus

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92
Q

What happens with cerebral edema and cytotoxic edema?

A

causes ischemic tissue
damages ATP pumps
often occur together

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93
Q

What are 3 examples of space occupying processes?

A

tumors, hematomas, abscess

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94
Q

What is hydrocephalus?

A

An accumulation of CSF

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95
Q

What are some clinical manifestations of increases ICP?

A

headaches, LOC changes, pupil changes, vomiting, vital signs, seizures, decreased motor function. posturing

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96
Q

WHat types of Vital sign changes would happen with increased ICP?

A

increased SBP
Decreased pulse
Altered RR pattern

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97
Q

What are the clinical manifestations of increased ICP in and infant?

A 
bulging fontanels
increases HC
HIgh pitched cry
poor feeding
sunsetting eyes
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98
Q

What is the treatment for ICP?

A

treat underlying cause
monitor, alleviate pressure (drain)
O2
Pharm

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99
Q

What is a seizure?

A

neurologic event with abnormal or excessive electrical discharges that can change motor function, sensation, autonomic visceral functions and behavior or consciousness

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100
Q

What are some reasons neonates would have seizures?

A

genetics, birth defects, infectons

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101
Q

The clinical manifestations of seizures depend on what 2 things?

A

What part of the brain it involved

and where it spread to

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102
Q

What kind of things can trigger a seizure?

A 
Stress
Lights
Stimuli
Infection
Fever
Lack of sleep
Constipation
head trauma
Drinking
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103
Q

What does epilepotogenic focus mean?

A

Where the seizure starts

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104
Q

What does prodromal/Aura mean?

A

having a subjective sense that seizure was going to happen

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105
Q

What does status epilepticus mean?

A

A seizure longer than 5 mins or back to back without recovery

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106
Q

What is a generalized seizure?

A

Involves entire brain

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107
Q

What is a Partial seizure?

A

involves part of brain surface

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108
Q

What does simple partial and complex partial mean?

A

simple- no impairment of consciousness

Complex- impairment of consciousness

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109
Q

What is the biggest sign of a generalized seizure?

A

loss of consciousness

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110
Q

What does a absence or petite mal seizure mean?

A

staring

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111
Q

What is a myoclinic seizure?

A

a single , or several jerks

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112
Q

What is a atonic seizure?

A

drop attacks/ falling down

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113
Q

What is a tonic clonic seizure?

A

jerking of many muscles

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114
Q

What is the treatment for seizures?

A 
Airway and safety
Document
treat cause
meds
avoid triggers
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115
Q

What are fibrile seizures?

A

Seizures accompanied by fever 100.4 or greater

NO CNS involvement

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116
Q

What is cushings triad?

A

Increased Systolic BP
Decreased pulse
Altered Resperations

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117
Q

What is the pathophisiology behind having diabetic ketoacidosis?

A

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

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118
Q

What are AED drugs?

A

Antiepileptic drugs

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119
Q

What are the two groups of AEDs?

A

Traditional and Newer agents

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120
Q

There are 6 different drugs in this category, generally have more drug interactions, have more intense AE but cost less. What group is it?

A

Traditional

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121
Q

There are 13 different meds in this category and are generally very expensive. What category?

A

Newer

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122
Q

This group of drugs are more tolerable and are safer during pregnancy .

A

Newer

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123
Q

What category of drugs should be avoided during pregnancy?

A

Traditional AEDs

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124
Q

What are the three most commonly used traditional drugs?

A

Phenytoin
Valproic Acid
Carbamazepine

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125
Q

What is the one type of seizure that phenytoin does not work for?

A

Absence seizures

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126
Q

How does phenytoin work?

A

Selective inhibition of sodium channels to prevent the entrance of sodium into hyperactive neurons

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127
Q

What is the half-life of phenytoin?

A

Depends on the does- smaller doses have smaller half life

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128
Q

Where is phenytoin metabolized?

A

in the liver- metabolism i limited

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129
Q

What is a normal loading dose of phenytoin? What route would be used?

A

15-20 mg/kg
IV - used while having a seizure or in coma
or PO

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130
Q

What are the maintenance doses of phenytoin?

What is the theraputic range? toxic?

A

Determined by plasma concentrations
10-20 mcg/mL
over 20 is toxic

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131
Q

What are the signs an symptoms of phenytoin toxicity?

A

Nystagmus, sedation, ataxia, diplopia, seizures

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132
Q

T/F

Phenytoin has a lot of adverse effects?

A

TRUE- it is a traditional AED and has many

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133
Q

What are the AE of phenytoin?

A

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

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134
Q

When phenytoin is given IV, what are some things to consider?

A

Cardiovascular effects- dysrhythmia, hypotension

INFUSE SLOWLY

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135
Q

What is the best way to administer phenytoin?

A

IV central access

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136
Q

What is fosphenytoin?

how is it administered?

A

It is converted into phenytoin in the body

ONLY IV

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137
Q

What are the benefits of using fosphenytoin vs. phenytoin?

A

It is easier to administer
less AE- does not cause purple glove
Can be infused faster

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138
Q

How much faster can fosphenytoin be infused?

A

3x faster

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139
Q

When giving fosphenytoin, even though it can be infused faster, it won’t work as fast- Why?

A

Needs to be converted before it can be utilized.

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140
Q

What is the biggest problem with phenytoin?

A

drug interactions

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141
Q

What types of seizures is carbamazepine used for?

A

partial and tonic-clonic

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142
Q

How does carbamazapine work in the body?

A

suppresses high-frequency neuronal discharge at foci

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143
Q

What are some interesting pharmacokinetics about carbamazeoine?

  • metabolism
  • loading dose
A

It is metabolized by liver b/c autoinduction
Half life decreases with continued therapy
No loading dose possible- slow increases needed

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144
Q

What are some AE of carbamazepine?

A

CNS - vision, dizziness (falls) **can build tolerance
Hematologic- bone marrow suppression (MONITOR)
TERATOGEN - spina bifida
Hyponatremia - Altered mental status/ unsteady
Dermatologic- rash, photosensitivity*

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145
Q

Why is valproic acid a bad option for people to take?

A

The frequency is too high 4x/dy

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146
Q

What are the three potential* MOA of divalproex?

A

sodium channel blockage
calcium channel suppression
inhibits GABA

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147
Q

What are the AE of divalproex?

A

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
Q

What are the drug interactions like with divalproex?

A

Complex- and have a synergistic effect with phenobarbital and phenytoin

149
Q

Why is Levetricetam such a good option?

A
  • used for many type of seizures
  • minimal drug interactions
  • mild to moderate side effects
  • IV or PO
150
Q

What is one of the most important things to remember when administering mannitol IV??

A

FILTERED TUBING

inspect- can crystalize

151
Q

What are some AE of mannitol?

A

Dehydration
decreased BP
decreased electrolytes
Serum osmolarity

152
Q

Mannitol is good for cerebral edma and getting fuild off the brain, why?

A

it is an osmotic diuretic

153
Q

What is the leading case of acute and chronic illness in children and the most frequent admitting diagnosis?

A

Asthma

154
Q

What are the 3 characteristic mechanisms of obstructive airway disease?

A

Bronchospasms
Inflammation and edema
reactivity to a variety of stimulli

155
Q

What are the high risk pops for asthma?

A

African american and hispanics
pops in inner-city
premature- low birth weights

156
Q

When does intrinsic asthma have its onset?

A

adult onset

with no history

157
Q

When does extrinsic asthma have its onset?

A

in childhood

158
Q

What is status asthmaticus?

A

Can’t get the asthma attack to stop

159
Q

What are the two responses of Asthma?

A

Early- inflammation

Late- 4-8 hrs later

160
Q

What is the pathophisiology of the early response of asthma?

A

Allergen binds to mast cell
mast cells degranulate and mediators are released (histamine)
Vasodilation and increased acetylcholine

161
Q

What causes the direct tissue damage in the late response of asthma?

A

eosinophils

162
Q

What is airway remodeling?

A

when there is chronic inflammation in the airway, the tissues are actually changed

163
Q

What three things happen with airway remodeling?

A

Basement membrane becomes thick
Mucous glads increase in numbers
Smooth muscles hypertrophy

164
Q

What are some severe clinical manifestations of asthma?

A 
cynosis
retractions, nasal flaring
decreased breath sounds
agitation
can't speak well
Decreased systolic pressure during inspiration
165
Q

What are the treatments for asthma?

A

manage allergens
peak flow meters
meds

166
Q

What is bronchiolitis?

A

inflammation of the brochioles- secondary to infection normally
Seasonal
Lower airway

167
Q

What is the pathophisiology behind bronchiolitis?

A

fibrin plugs
air trapping- hyperinflation
increased work of breathing

168
Q

What are the clinical manifestations of bronchiolitis?

A 
Rhinorrhea and tight cough
decreased appetite, lethergy, fever
tachypnea- retractions 
abnormal sounds 
hyperexpanded
169
Q

What is the treatment for bronchiolitis?

A

supp O2
increased hydration
inhaled hypertonic saline
NG tube feeds

170
Q

Virchow’s triad

A

Vessel wall injury
circulatory stasis
hypercoagulable conditions

171
Q

What are the two first clinical manifestations you will see when someone has a pulmonary embolism?

A

DYSPNEA

restlessness, apprehension and anxiety

172
Q

What are two short acting inhaled bronchiodilators?

A

Albuterol and Ipratropium

173
Q

Which type of inhalation med has less systemic side effects?

A

DPI- dry powder

174
Q

corticosteriods will help decrease what?

A 
Inflammatory cells and Structural cells** 
cytokines
mast cell numbers
macrophage numbers
mucus secretions
175
Q

beclomethosone

A

Inhaled corticosteroid
minimal systemic absorption
can be MDI

176
Q

What are the most common AE of beclomethasone?

A

Oral candidiasis
Dysphonia- crackle talk
promotes bone loss
rinse mouth

177
Q

Albuterol

A

inhaled brochodilator
Beta- agonist
short acting- used for exercise induced
Immediate use-last 30 to 60 mins

178
Q

Ipratropium

A

Inhaled bronchodilator
Anticholingerics- blocks muscarinic receptors
short actingmay last for 6 hrs

179
Q

What are the AE of albuterol?

A

tachycardia, tremor, hypokalemia

180
Q

What are the AE of Ipratropium?

A

minimal systemic
dry mouth
pharyngeal irritation

181
Q

Montelukast

A

*controller med
supresses leukotrines
Oral BID- or 2 hrs before workout

182
Q

What are the 4 broad types of genetic disorders?

A

Chromosomal anomalies- number and structure
Single-Gene disorder- dom/rec.x-link
Polygenic/multifactoral
Other

183
Q

What is it called when someone has anything other than 46 chromosomes?

A

aneuploidy

184
Q

Between a sex linked anomaly and a monosomy, which is more dangerous and debilitating?

A

Sex inked is more common and less troubling but monosomy is more problematic

185
Q

What are the 5 types of abnormal structures?

A 
Deletion
Duplicates
Inversions
Insertion
Translocations
186
Q

What is translocation?

A

One part of chain is flipped

187
Q

What is a point mutation?

A

Substitution of a single base pair and either does/doesn’t change amino acid

188
Q

What is a frameshift mutation?

A

addition or deletion of 1 or 2 nucleotides

* changes all codons after the shift

189
Q

Autosomal Recessive Disorder

A

AA-none
Aa-carrier
aa- affected
**unaffected can still pass if they carry

190
Q

Autosomal Dominant Disorder

A

AA- Affected
Aa- Affected
aa-none
**unaffected do not pass it

191
Q

What is an example of autosomal dominant disorder?

A

huntingtons disease

192
Q

What is another name for AA?
Aa?
aa?

A

Homozygous Dominant
Heterozygous
Homozygous Recessive

193
Q

What gender sees x-linked recessive more?

A

males

194
Q

What are 2 examples of x-linked recessive ?

A

Hemophilia A

Duchenne Muscular Dystrophy

195
Q

What are polygenic traits?

A

traits that are a result of several genes acting together

196
Q

What are multifactorial ?

A

Genes thar makes someone susceptible

197
Q

What is penetrance?

A

phenotype associated with genotype

** reason why it may skip generations

198
Q

What is expressivity?

A

Extent of variation- environmental factors and other genes

199
Q

Down Syndrome

A

trisomy 21
nondisjunction
translocation
mosaicism

200
Q

Duchenne muscular dystrophy ?

A 
only males
by age 3 
deficient in protein 
leaks creatinine 
necrosis/degeneration
gradual loss
201
Q

Sickle cell affects which chromosome?

A

11- point mutation

202
Q

What are some triggers for sickle cell crises?

A

Dehydration, cold, infection, hypoxia, fever, acidosis

203
Q

What are the two parts of sickle cell anemia?

A

Sickling- occlusion-stickin, pain, tissue damage

Anemia- short lifespan, hyperbilirubinemia

204
Q

What are the two inflammatory bowel diseases?

A

Ulcerative colitis and chron’s disease

205
Q

What is the definition of ulcerative colitis?

A

inflammatory disease of the mucosa of the colon and rectum

206
Q

When ifs the onset of the inflammatory bowel diseases?

A

childhood and young adulthood

207
Q

Chrons disease affects what part of the GI?

A

Mouth to anus, has skip lesions so it may affect a different part with exacerbations

208
Q

UC affects what part of the GI?

A

Large intestines, continuous

209
Q

Which inflammatory disease has a cobble stone apperance and why?

A

Crohns disease has a cobble stone appearance because of the granulomas

210
Q

What are some of the factors for inflammatory diseases?

A

jewish decent, family history, white, immunological factors, environmental factors

211
Q

What starts the process of UC in the GI system?

How does it continue?

A

1-Inflammation at base of crypts- activated neutrophils and macrophages
2-abscess formation
3-abscessess come together and form ulcers
4-repair- fragile

212
Q

What are some clinical manifestations of UC?

A

diarrhea because of a lack of ability to absorb water
rectal bleeding
pain in abdomen

213
Q

How would UC be diagnosed?

A

Hx-P

Biopsy- ulcers

214
Q

What is used to treat UC?

A

corticosteroids
immunosuppresants
nutritional management
antibiotics

215
Q

What types of nutritional changes would someone with UC have to incorporate?

A

no milk, low fiber, low fat, increase protein

216
Q

What part of the GI system does Chrons affect?

A

Mouth the anus, but there are skip lesions, so not all will be affected at once

217
Q

What is the cardinal feature of Chrons?

A

Granulomas

218
Q

What starts the exacerbation of Chrons?

A

1-blockage of the GI lymphoid and lymphatic structures
2-Engorged//inflammed= deep ulcers
3-tickened by fibrous scor, deep fistulas-openings

219
Q

What are the clinical manifestations of Chrons?

A

incapable of adequately absorbing nutrients -weight loss, malnutrition, hight/wt

  • skipping lesions
  • perianal fissures, fistulas and abscesses
220
Q

In what situation would someone with inflammatory bowel need to get a colectomy?

A

if there was high grade dysplasia

221
Q

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?

A

Chron’s Disease

222
Q

When someone tells you they have bloody stools an diarrhea on many occasions, what type of inflammatory bowel would you think they have?

A

Ulcerative colitis

223
Q

Malabsorption is more common with with IBD?

A

Chron’s Disease

224
Q

What age group is GERD most likely to affect?

A

0-6 moths and adults

225
Q

What is the definition of GERD?

A

backflow of gastric contents into the esophagus through the lower esophageal sphincter (LES)

226
Q

What are the three broad causes of GERD?

A

1- issues with LES- strength and efficacy
2- increases in intraabdominal pressure
3- delayed gastric emptying

227
Q

What are some examples/reasons of GERD as a result of LES issues?

A

high fat diet, caffeine, alcohol, smoking, obesity and meds

228
Q

What are some examples/reasons of GERD as a result of intraabdominal pressure?

A

pregnancy, constipation, tumor, overfeeding, crying

229
Q

What are some examples/reasons of GERD as a result of delayed gastric emptying?

A

being an infant

230
Q

What are some clinical manifestations of GERD?

A

heartburn, regurgitation, chest pain, dysphasia.

infants often will not have symptoms- physiologic reflex

231
Q

What are two complications of GERD?

A

1-aspiration- asthma, coughing, laryngitis

2- highly acidic in esophagus - structures, narrowing

232
Q

What is some treatment for GERD?

A

diet/behavior- low fat diet, low caffeine, and no smoking
Antacids and histamine blockers
proton pump inhibitors.

233
Q

What are some treatment options for infants with GERD?

A

small frequent meals and burping
thickened feeding controversial
positioning
meds

234
Q

What are some common presenting symptoms of GERD in infant patients?

A 
feeding refusal, 
recurrent vomiting
irritability
poor weight gain
sleep problems
resp symptoms
235
Q

What are some common presenting symptoms of GERD in older children or adolescent patients?

A 
abd pain and heartburn
vomiting
dysphagia
asthma
pneumonia
upper airway symptoms
236
Q

What is osteomyelitis?

A

Severe infection of bone and local tissue

237
Q

What are the two most common organisms of osteomyelitis?

A

staph aureus

strep pneumaniae

238
Q

what are the three ways osteomyelitis can reach the blood?

A

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

239
Q

Who are people at high risk for osteomyelitis?

A

those who have had surgery- contamination
open fractures
IV drug users
kids less than 16 and older adults

240
Q

What is the treatment for osteomyelitis?

A

4-6 weeks of IV antibiotics OR IV to oral
debridement if needed
removal of prosthesis or other materials

241
Q

How would osteomyelitis be diagnosed?

A

X-ray,
increased WBC, CRP, ESR- inflammation and infection
bone scan
blood cultures and bone aspirate

242
Q

What are the differences in pediatric bones?

A

less brittle, higher collagen to bone ratio
Stronger periosteum
Presence of epiphyseal plate

243
Q

What would you expect the X-ray of a comminuted bone fracture to look like?

A

Fragments of broken bones

244
Q

What is an epiphyseal fracture?

A

a break through the growth plate of a bone

245
Q

What is the process of healing of a cortical bone?

A 
Bleeding
Hematoma
Osteoblasts and calcium
Callus formation
Callus reabsorbed
246
Q

What are the assessments for compartment syndrome ?

A 
5 Ps
pain
paralysis
parasthesis
pallor
pulses
247
Q

What are some complications of a fracture?

A 
delayed healing
compartment syndrome
fat embolism syndrome
osteonecrosis
osteomyelitis
DVT
neurovascular injury
248
Q

What is Ranitidine also known as?

A

Zantac

249
Q

What is Zantac used for?

A

It is a histamine2 receptor antagonist
Oral and IV
OTC and Rx

250
Q

What are two things users of Zantac should know?

A

Caution in pregnancy

Drug interactions!

251
Q

What is Omeprozole also known as?

A

Prilosec

252
Q

What does Omeprozole do in the body?

A

irreversible Inhibits the proton pump
blocks gastrin production
*PO or IV
OTC or Rx

253
Q

What is a long-term effect of Omeprozole?

A

increases risk of osteoporosis= increased fracture risk- decreased absorption of calcium

254
Q

What are some increased risks when taking omeprozole?

A

Pneumonia
C-diff
Dementia
Kidney injury

255
Q

Surcralfate is what type of drug?

A

Mucosal protectant

256
Q

How does Sucralfate work?

A

Adheres to ulcer for up to 6 hours to protect and prevent more damage

257
Q

What are some AE of Sucralfate?

A

constipation
can decrease absorption of other meds
*caution in pregnancy

258
Q

Milk of Magnesia is also called ____?

A

magnesium hydroxide

259
Q

What is the proper name for tums?

A

calcium carbonate

260
Q

MOM and tums are used for what?

A

neutralize gastric acid and inactivate pepsin

*potential mucosal protectant

261
Q

What are the AE of Antacids?

A

constipation and diarrhea

262
Q

What should people taking antacids be aware of?

A
  • caution in pregnancy
  • avoid with GI perforation or obstruction
  • caution with renal dysfunction
263
Q

What are some ways to treat IBD?

A 
5-aminosalicylates
Glucocorticoids
Immunosuppressants
Immunomodulators
Antibiotics
264
Q

What are the mild treatment options for UC according to the pyramid?

A

Topical or oral aminosalicylates

Probiotics

265
Q

What are the moderate treatment options for UC according to the pyramid?

A

immunomodulators
corticosteroids
Infliximab

266
Q

What are the severe treatment options for UC according to the pyramid?

A 
Colectomy
Inflixamab
Antibodies
cyclosporine
Experimental Rx
267
Q

What are the mild treatment options for Chron’s according to the pyramid?

A

Antibiotics
Aminosalicytates
budesonide
fish oil- probiotics

268
Q

What are the moderate treatment options for Chron’s according to the pyramid?

A

Inflixamab
Immunomodulators
corticosteroids
methotrexate

269
Q

What are the Severe treatment options for Chron’s according to the pyramid?

A

Surgery
Adalimemab
clinical trials

270
Q

Sulfasalazine is what type of drug and how does it work?

A

5-aminosalicylate

Decreases inflammation by inhibiting prostaglandin synthesis

271
Q

What are some AE of Sulfaslazine ?

A

Blood disorders and anemia

272
Q

where is sulfasalazine metabilized?

A

in the intestinal flora

273
Q

How is sulfasalazine administered?

A

Oral or Rectal-enema or suppository

274
Q

What are 5 types of drugs most commonly used for mental health?

A

1- Selective Seratonin Reuptake Inhibitors SSRIs
2- Tricyclic Antidepressants TCAs
3- Serotonin-Norepinephrine Reuptake Inhibitors
4- Atypical Antidepressants
5- Benzodiazapines

275
Q

What is an example of an SSRI?

A

Paroxetine- Paxil

276
Q

What is an example of a TCA?

A

Nortriptyline

277
Q

What is an example of Serotonin-norepinephrine reuptake inhibitor?

A

Venlafaxine- Effexor

278
Q

What is an example of atypical antidepressant?

A

Bupropoin- Wellbutrin

279
Q

What is an example of a benzodiazapine?

A

Alprazolam- Xanax

280
Q

When taking Paroxetine, what are some things you should know?

A

*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
Q

What would be some indicators that you have serotonin syndrome?

A

muscle rigidity
fever
altered mental syndrome

282
Q

When taking SSRIs, what other drugs should you be aware of?

A

Anything that has an antiplatelet agent

283
Q

What type of mental health drugs are fairly dangerous and have lethal toxicity problems?

A

TCAs

284
Q

What is an example of a TCA?

A

Amitriptyline

285
Q

What is Amitriptyline most commonly used for?

A

Sleep and neuropathic pain

*not for depression

286
Q

How does Amitriptyline work?

A

blocks neuronal reuptake of NE and serotonin

287
Q

What are the significant side effects of Amitriptyline?

A 
Orthostatic hypotension
sedation
anticholinergic effects
cardiac toxicity
Seizures
288
Q

What is an example of serotonin-norepinephrine reuptake inhibitor?

A

Venlafaxine

289
Q

How does Venlafaxine work?

A

Blocks the reuptake of NE and serotonin- Similar to SSRIs

290
Q

What are the adverse effects of Venlafaxine?

A

Weight gain, HA, insomnia, dizziness, sexual dysfunction, serotonin syndrome, hypertension and tachycardia

291
Q

What two types of drugs should somene taking serotonin-norepinephrine reuptake inhibitor be careful of taking together?

A

NSAIDs and anticoagulants

292
Q

What is an example of a drug used for atypical antidepression and what is it used for?

A

Bupropion

used for smoking

293
Q

What are some adverse effects of Bupropion?

A 
agitation
HA, dry mouth
constipation
weight loss
Serious= Seizures
294
Q

How many types of formulations does Bupropion have?

A

3
immediate
sustained
XL tabs

295
Q

How long will it take for a response to antidepressants?

A

weeks

*max response at 3 months

296
Q

What is the MOA of benzodiazapines?

A

intensifies GABA

297
Q

What are the effects of Benzos?

A

reduced anxiety
promotes sleep
muscles relaxant
**can have withdrawal symptoms

298
Q

What is an example of a benzodiazapine?

A

Alprazolam

aka Xanax

299
Q

What are the AE of Xanax?

A

CNS depression
Respiratory depression
Anterograde amnesia

300
Q

What is the goal of medical treatment for heart failure?

A

To prevent and decrease damage to heart

301
Q

What is the last line of medication used for heart failure?

A

inotropic support which improves contractility

302
Q

What two types of drugs have damaging effects on the myocardium?

A

Catecholamines and angiotensin 2

303
Q

What type of diuretics would you use if you wanted a big effect?

A

Loop diuretics

304
Q

When taking a diuretic for symptom management, what type would you take?

A

Loop diuretics

305
Q

What is an example of a loop diuretic?

A

furosemide aka lasiks

306
Q

What is the biggest AE to be aware of when taking furosemide?

A

hypokalemia

also, hypotension

307
Q

What two types of diuretics are commonly used together and why?

A

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
Q

What is an example of a potassium sparing diuretic?

A

spironolactone

for mild diuresis

309
Q

What is an example of thiazide diuretics?

A

Hydrochlorothiazide

310
Q

What are the AE of hydrochlorothiazide?

A

hypokalemia and hypertension

311
Q

What are the AE of spironolactone?

A

hyperkalemia and gynecomasita in men

312
Q

If a patient has poor GFR, which type of diuretic do you know will still work?

A

loop diuretics

313
Q

What is an example of an ACE inhibitor?

A

lisinopril

314
Q

By blocking the ACE, what are you doing and preventing overall?

A

Decreasing mortality, improving function and preventing remodeling= angio1–angio2–vasoconstriction to remodeling

315
Q

What are the AE of lisinopril?

A

angioedema, cough and hyperkalemia

316
Q

What is an example of an angiotensin II receptor blocker?

A

losartin

317
Q

What are the AE of losartin?

A

hyperkalemia and less angioedema

318
Q

What are the beniftis of taking an angiotensin II receptor blocker?

A 
improve LV EF
reduce symptoms
increase exercise tolerance
decrease hospitalizations
enhance QOL
reduce mortality
319
Q

If someone were to have severe heart failure, which drug would be best?

A

Losartin

320
Q

Why would you not want to give someone with hear failure amlodapine?

A

Causes peripheral edema and you don’t want edema with heart failure patients

321
Q

What type of drug would you want to use, add, later own the heart failure road?

A

aldosterone antagonist- spironolactone

322
Q

Beta blockers can do what 5 things?

A 
improve LVEF
increase exercise tolerance
Slow progression of HF
Reduce need for hospitalization
Prolong survival
323
Q

What is an example of a cardiac glycoside?

A

Digoxin

324
Q

What is the biggest effect that digoxin has that can also cause many of the AE?

A

Inhibits Na-K- ATPase pump=hypokalemia, hyperkalemia

heart dysrhythmias

325
Q

What are some AE of digoxin?

A 
Heart dysrhythmias
anorexia
nausea 
vomting
halo- visual disturbances

many drug interactions

326
Q

What is an example of a vasodilator?

A

Hydralazine

327
Q

What does hydralazine do?

A

selective dilation of arterioles

*combo with nitrates

328
Q

NItroglycerin is commonly used for what?

A

chest pain- dilates veins and decreases venous return and decreases O2 demands

329
Q

Why have there been deaths from nitro?

A

drastic drop in BP

330
Q

What is the foramen ovale?

A

the whole between the R atrium and L atrium- closes after birth

331
Q

What is the ductus arteriosus?

A

The the shunt from the pulmonary artery to the aorta- bypass the lungs

332
Q

What are some environmental reasons someone would get a congenital heart disease?

A 
infections
metabolic disease
drug exposure
alcohol
increase maternal age
333
Q

What are the two ways CHD is classified?

A

Cyanotic and Acyanotic

  • Blood flow to lungs
  • obstruction
  • mixed blood
334
Q

What CHD are acyanotic and have increased pulmonary bloodflow?

A

PDA, ASD & VSD

335
Q

What CHD is an obstruction?

A

coarctation of the aorta

336
Q

What CHD had a decrease in pulmonary blood flow?

A

Teralogy of Fallot

337
Q

What CHD has mixed blood flow?

A

Transposition of the great arteries

338
Q

What side of the heart has a greater pressure gradient ?

A

left

339
Q

If the heart is having to work harder than normal What will happen to the muscle?

A

hypertrophy

340
Q

What is PDA?

A

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
Q

Where is the workload going to in PDA?

A

workload to the lungs= pulmonary hyepertension and right sided heart failure

342
Q

What med is given to close the opening from PDA?

A

Indomethacin

343
Q

What are some clinical manifestations of PDA?

A

murmur
widened pulse pressure
bounding pulses

344
Q

What is ASD?

A

opening in the septum between the aorta and right atrium -foramen ovale

345
Q

whre is the workload in ASD?

A

right sided with right sided failure

346
Q

Where is the pressure in the heart with ASD?

A

in the right. Blood moves from aorta to right atrium

347
Q

What are some clinical manifestations of ASD?

A

fatigue, dyspnea with exertion, resp infections, murmur

348
Q

What is coarctation of the aorta?

A

Narrowing of the aorta

*most common around ductus arteriosus

349
Q

Where is the workload with Coarctation?

A

left sided-with hyertrophy

*pulmonary manifestatins

350
Q

What are some clinical manifestations with coarctation of aorta?

A

murmur
poor lower extremity perfusion
pulse and BP differences in upper and lower
Initial L sided heart failure

351
Q

What drug is given to keep ductus arteriosus open?

A

prostaglandin E

352
Q

What 4 things are wrong with tetralogy of fallot?

A

VSD
Overriding aorta- crossover to both ventricles
Pulmonary stenosis
RV hypertrophy

353
Q

Where is the workflow in Tetralogy?

A

Right sided –> pulmonary stenosis

354
Q

What are some clinical manifestation of Tetralogy?

A

Cyanosis, fatigue
murmur
tet spells
boot shaped heart on XRAY

355
Q

What is a tet spell and what happens?

A

normally will happen when people eat, cry, poop= more unoxygenated blood out to the body= blue

356
Q

What is transposition of the great arteries?

A

The aorta and pulmonary artery are switched

**not compatable with life

357
Q

Pathologically, what is happening to the blood with transposition?

A

The RV is sending unoxygenated blood to the body

The LV is sending oxygenated blood to thr lungs

358
Q

What three things do you want to control when managing CHF?

A

Stroke volume

  • Preload
  • contractility
  • afterload
  • heart rate
359
Q

What is happening with systolic heart failure?

A

ventricles don’t pump enough blood out

low EF

360
Q

What is happening with diastolic heart failure?

A

Ventricles don’t fill properly

361
Q

What are clinical manifestations of left sided heart failure?

A 
Dyspnea, orthopnea
cough
crackles
hemoptysis
Tachy
cool, pale
362
Q

What are clinical manifestations of right sided heart failure?

A

Jugular vein distestion
Hepato-splenomegaly
Weight gain, edema

363
Q

What drug helps improve cardiac output?

A

digoxin

364
Q

What type of drugs help minimize congestive symptoms ?

A

diuretics

365
Q

With depression, Where is pharm most focused?

A

within the deficiency of monoamines

366
Q

What is the monoamine deficiency theory?

A 
Not as much in synaptic space
1- decrease in baseline neurotransmitters
2- overactive reuptake
3- Enzymes
4- Transporters are low

Pharm/Patho (6 decks)

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