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NURS 709 Pathophysiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is considered the upper respiratory tract?

A

Throat up

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2
Q

What is considered the lower respiratory tract?

A

Throat down

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3
Q

What causes the viral common cold?

A

Rhinoviruses
Parainfluenze
RSV
Adenoviruses

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4
Q

What are the symptoms of the viral common cold?

A

The viral common cold is self limiting
Increased secretions
Sore Throat
HA
Fatigue
Post-nasal drip

(Symptoms are normally from the throat up)

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5
Q

How long does the viral common cold last?

A

Normally runs its course in 7 days with an incubation period of 2 days

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6
Q

How are viruses spread?

A

By Contact (fingers)
Portal of Entry (nasal mucosa and conjunctival surfaces)

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7
Q

What is the progression of Rhinosinusitis?

A

Viral URI/allergic rhinitis leads to mucousal swelling which leads to ostia obstruction and impaired mucociliary clearance

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8
Q

What are other non-viral causes of rhinosinustitis?

A

Bacterial
Swimming
Driving
Abuse of nasal decongestants

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9
Q

How is rhinosinusitis classified?

A

Classified as acute or chronic
Acute is equal or under 4 weeks
Chronic is over 12 weeks

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10
Q

What are the clinical manifestations of rhinosinusitis?

A

Purulent nasal drainage
Decreased sense of smell and fever

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11
Q

A fever can distinguish what about rhinosinusitis?

A

Whether the cause is bacterial or viral

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12
Q

Influenza is caused by?

A

The influenze virus NOT a bacteria

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13
Q

Where in the respiratory tract does the flu affect?

A

Both upper and lower

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14
Q

Where does influenza target and what is it’s method of action?

A

Influenza targets and kills mucous-secreting ciliated epithelial cells, creating holes in the basal membrane cells.
Extracellular fluid escapes which causes a runny nose

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15
Q

What are the 3 types of RNA single strand viruses?

A

A, B, C

Type A viruses are further divided by H(1-18) and N(1-11) subtypes (Surface glycoproteins)

Pandemic Influenzas

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16
Q

How is influenzas spread?

A

inhalation of droplets

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17
Q

What is H(1-18)?

A

hemoglutenin antigen on surface of viruses

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18
Q

What is N(1-11)?

A

Enzymes that predicts how well a virus can replicate

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19
Q

What are the systemic manifestations of the flu?

A

Body aches, fatigue, headache, fever, chills

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20
Q

What is the onset and duration typically of influenza?

A

Acute onset, malaise over a morning.
Symptoms peak by day 3-5, and disapears by 7-10 with an incubation period of 1-2 days

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21
Q

What are the possible complications of influenza?

A

Pneumonias
Exacerbation of pre-existing respiratory disorders

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22
Q

Who is at the highest risk of complications from the flu?

A

Children/elderly
Pts with pre-existing respiratory disorders
Immunosuppressed persons
Pregnant women
Morbidly obese persons

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23
Q

Who is the flu vaccine recommended for?

A

all people 6 months and older

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24
Q

What is the treatment for the flu?

A

Antiviral drugs are available if taken in first 48 hours
Treatment is symptomatic/supportive:
Rest, antipyretics, hydration, cough syrups/drops

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25
Q

What is pneumonia?

A

Inflammation of the lung parenchyma often due to an infectious agent (typically bacteria)

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26
Q

What are the classifications of pneumonia?

A

By organism
By distribution of infection
Community or hospital aquirred

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27
Q

What are the risk factors for pneumonia?

A

Very young/very old
Chronic illness
Prolonged immobility
Immunosuppression
Alcoholism
Malnutrition
Inhalation of fumes or gastric contents

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28
Q

Community acquired pneumonia is?

A

Infections contracted outside the hospital

S. pneumoniae is most common agent (H. Infkuenzae and S. aureus can also be causes)

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29
Q

What is hospital acquired/nosocomial pneumonia?

A

Infections that occur 48 hours or more after admission to an inpatient facility

Mostly bacterial (Pseudomonas, S. aureus, Enterobacer, E. Coli)

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30
Q

What is the diagnosis/treatment of pnuemonia?

A

H&P
Chest Xray
Sputum
Blood Cultures
Appropriate antibiotic therapy

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31
Q

Streptococcal pneumoniae aka pneumococcus is?

A

A mostly bacterial pneumonia 75% community acquired, with sudden onset

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32
Q

What is streptococcal consolidation?

A

Fluid or exudate fills groups of alveoli displacing air

Visible on xray, this edema reduces ventilaton and impairs gas diffusion

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33
Q

What are the signs and symptoms of streptococcal pneumonia?

A

Chills/high fever
Pleural pain
Cough
Bloody sputum
Hypoxemia
Cyanosis (need to be admitted to the hospital)

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34
Q

How is streptococcal pneumonia treated?

A

with antibiotics, however resistance can occur

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35
Q

What are the 4 stages of streptococcal pneumonia?

A

Edema
Red hepatization (living tissue looks red and bloody)
Grey hepatization
Resolution

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36
Q

What disease is the world’s foremost cause of death from a single infectious agent?

A

Tuberculosis

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37
Q

Where is TB more common?

A

It is more common among recent immigrants from areas with high rates an those living in congregate settings

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38
Q

What is the infectious agent responsible for TB?

A

Mycobacterium tuberculosis which is a aerobic mycobacteria that is contracted through inhalation of bacilli

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39
Q

What helps prevent destruction of the mycobacterium tuberculosis?

A

It has a waxy coating that helps prevent destruction plus acid fast bacilli

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40
Q

How is TB spread?

A

The mycobacterium is exhaled in the respiratory secretions of individuals with active TB

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41
Q

What are the two categories of TB?

A

Primary/Active TB (10%)
Latent TB(LTBI-90%)

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42
Q

What is primary/active TB?

A

Previously unexposed and unsensitized person contracts TB

Bacteria is dividing in body, mostly in lungs

Progressive TB is usually symptomatic and infectious

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43
Q

What is latent TB?

A

The cell mediated response has halted TB replication, TB bacteria are localized in small lesions

Most people develop after Primary TB
Asymptomatic, NOT infectious

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44
Q

What is a Mantoux tuberculin test?

A

0.1cc PPD of TB is injected intradermally

48-72 hours later, site is examined for induration

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45
Q

What are the cutoffs for the size of the induration diameter?

A

Size of induration diameter cutoff is based on certain risk factors but is 5mm, 10mm and 15mm to the general public

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46
Q

What is a QuanitFERON-TB Gold test?

A

A test that measures interferon-y that has a 24 hour result turnaround and can test for LTBI

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47
Q

What is TB treatment?

A

Antimycobacterial drug treatment:n
A multidrug therapy that lasts for 9 months that eliminates all tubercle bacilli

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48
Q

What is the follow-up after TB treatment?

A

CXR screens for lung involvement
Can test sputum samples for the mycobacterium

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49
Q

What is the etiology of COVID19?

A

Infection with SARS-CoV-2 a coronavirus with numerous variants such as Omicron, Delta, etc.

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50
Q

Which variant of Covid-19 spreads the fastest?

A

Omicron

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51
Q

How are Covid 19 variants named?

A

Names come from spikes on the virus

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52
Q

What are the types of testing for Covid-19?

A

Nucleic acid amplification tests (PCR testing)
Antigen testing

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53
Q

What are the 4 Authorized vaccines in the US?

A

Pfizer (mRNA)
Moderna (mRNA)
Novavax (protein subunit vaccine)
Johnson & Johnson (viral vector)

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54
Q

Type 1 diabetes is?

A

Diabetes that usually has a juvenille onset where Beta cells are destroyed

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55
Q

Type 2 diabetes is?

A

The most common type of diabetes with a traditionally adult onset where cells begin to gradually become insulin resistant

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56
Q

What is pre-diabetes?

A

Patients who have a higher average glucose but is not yet diabetic

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57
Q

What is gestational diabetes?

A

Pregnancy related diabetes that occurs in 2nd or 3rd trimester

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58
Q

What is the pathophysiology of Type 1 diabetes?

A

Little or no insulin due to Beta cells in pancreas being destroyed through autoimmune destruction of islet cells

When no insulin is present, the body breaks down fats and proteins

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59
Q

What are the Characteristic of Type 1 diabetes?

A

Catabolism of muscle
Development of ketosis
Onset in childhood and adolescence
Requires insulin therapy

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60
Q

How is type 1 diabetes normally discovered?

A

A severe episode normally causes patient to see care

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61
Q

What are the important risk factors for Type 2 diabetes?

A

Obesity
Fat Distribution (Trunkle obesity=increased risk)
Lack of physical activity

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62
Q

What is the pathophysiology of Type 2 diabetes?

A

-Gradual insulin resistance of the target cells
-May involve impaired insulin secretion
-Increased glucose production from liver

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63
Q

How insulin secretion impaired in type 2 diabetes?

A

The body, in response to insulin resistance, will begin to produce more and more insulin and eventually pancreas will ‘give up’ and we will see increased glucagon by the liver

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64
Q

What are the characteristics of Type 2 diabetes?

A

-Onset usually occurs after age 40
-Often in overweight/obese individuals
-May require insulin therapy if lifestyle changes are not enough to manage

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65
Q

What is the difference in the timing of onset between type 1 and tyoe 2 diabetes?

A

Type 1-abrupt onset, symptomatic
Type 2-gradual onset, subtle, often asymptomatic

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66
Q

What is Metabolic Syndrome?

A

A group of problems in body that are all related to impaired metabolism that involve manifestations of abnormal lab values, vital signs, body weight and have a strong association with atherosclerosis and general arterial disease

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67
Q

What are the components of metabolic syndrome?

A

Increased BP (130/85 or higher)
High Triglycerides (150 mg/dL or more)
Large waistline (Men 40”, Women 35”)
Low LDL(Men 40, women <50)
Elevated fasting blood sugar (100mg/dL)

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68
Q

What are the two most common test for diabetes?

A

Fasting plasma Glucose
Hemoglobin A1c%

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69
Q

What are the requirements to be diagnosed with diabetes?

A

2 Fasting plasma glucose levels of >126mg/dL

HbA1C >6.5%

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70
Q

What is the level of Fasting plasma glucose to be considered to have pre-diabetes or impaired FPG?

A

100-125 mg/dL

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71
Q

What is the HbA1C level to be considered to have prediabetes?

A

5.7-6.4%

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72
Q

How does a high HbA1C effect circulation?

A

Erythrocytes get coated in glucose, and makes the RBC stiff, loosing their flexibility which creates circulation problems

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73
Q

What is the monitoring of diabetes?

A

Pts. self monitor with ‘fingersticks’ for FPG or Random glucose checks

HbA1C checked every 3-4 months

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74
Q

How many people in the US have diabetes?

How many have prediabetes?

A

34.2 million people (10.5% of US population)

88 million (34.5% of the adult US population)

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75
Q

What are the acute complications of DM?

A

Diabetic Ketoacidosis
Hyperosmolar Hyperglycemic State
Hypoglycemia

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76
Q

What is the development of Diabetic Ketoacidosis?

A

Lack of glucose->

Cells break down triglycerides in free fatty acids for gluconeogenesis->

Oxidation of FFA leads to increased ketones->

Metabolic acidosis ensues as the ketones deplete the ECF and cell buffer systems->

Diuresis occurs, loosing K, Na, phosphates and water

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77
Q

What are the manifestations of DKA?

A

PG>250 mg/dL
Low arterial pH
Kussmaul’s respirations
Acute onset
Malaise
Headache
N/V/D
Stupor
Coma
Hypotension
Tachycardia

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78
Q

What are the manifestations of Hyperosmolar hyperglycemic state?

A

More common in type 2:

Hyperglycemia (PG>600mg/dL)
Hyperosmolarity (Serum osm >320)
Polyuria->Dehydration
Normal pH levels

(symptoms of a fluid volume deficit)

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79
Q

What is hypoglycemic insulin shock?

A

Significant drop in plasma glucose
Most common in pts taking insulin

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80
Q

What are the symptoms of hypoglycemic insulin shock?

A

Headache
Reduced LOC
Seizures/coma
Anxiety
Tachycardia
Diaphoresis

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81
Q

What are the long term complications of Diabetes?

A

Retinopathy
Nephropathy
Neuroparthy
PAD
MIs
CVAs
Foot ulcers
Increased susceptibility to infections

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82
Q

What is diabetic retinopathy?

A

Long term elevated blood sugar causes the tiny capillaries in the retina to have ischema

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83
Q

Diabetic nephropathy is?

A

The most common cause of end stage renal disease where protein leaks into urine starting with microalbumin and leading to hypoproteinemia later

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84
Q

What is diabetic neuropathy?

A

Nerves no longer transmit properly->
Axonal degeneration due to high PG
Sensory nerve injury precedes motor nerve injury

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85
Q

What is endocrine hypofunction?

A

impaired development of a gland

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86
Q

What is endocrine hyperfunction?

A

Excessive hormone production

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87
Q

What is the cause of endocrine hormone resistance?

A

receptor defects

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88
Q

What are the levels of endocrine disorders?

A

Primary
Secondary
Tertiary

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89
Q

What is a primary endocrine disorder?

A

The problem originates in the target endocrine gland

90
Q

What is a secondary endocrine disorder?

A

The problem is the gland not producing enough hormone

91
Q

What is a tertiary endocrine disorder?

A

The problem results form hypothalamic dysfunction

92
Q

What are the two categories of pitutary tumors?

A

Primary and Secondary Tumors
Functional tumors->hyperituitarism and are found in anterior pituitary
Nonfunctional tumors

93
Q

What is hypopituitarism?

A

Decreased secretion of pituitary hormones that can be congenital or acquired

ACTH Deficiency is the most serious

94
Q

What are the symptoms of hypopituitarism?

A

Normally they start gradually but can become life threatening:
Weakness
Fatigue
Loss of Appetite
Cold Intolerance

95
Q

What are the physical findings of growth hormone deficiency in children?

A

Pituitary dwarfism
Increased subQ fat
Immature facial features

96
Q

What can be a cause for a growth hormone deficency?

A

Pituitary tumors

97
Q

What is the cause for growth hormone excess in children?

A

Usually caused by pitutary adenomas
Results in excessive skeletal growth

98
Q

What are the two classes of immunodeficiency states?

A

Primary (congenital or inherited)
Secondary (acquired later in life)

99
Q

What are some of the factors that could contribute to acquiring a secondary immunodeficency?

A

Malnutrion (esp protein deficences)
Infection (think AIDS)

Neoplastic Diseases (Lymphoma)

Immunosupressive Therapy
(corticosteroids or transplant rejection meds

100
Q

Besides primary and secondary, we can divide immunodeficences into what?

A

Humoural vs Cell mediated

101
Q

What would be considered a humoural immunodeficency?

A

Malnutrition
Major burns
Nephrotic syndrome (protein loss through urine)

102
Q

What would be examples of cell mediated immunity?

A

Hodkin’s Lymphoma
Viral infections like HIV

103
Q

What type of disorders account for 70% of primary immunodeficencies?

A

Humoral (B lymphocyte) disorders

104
Q

What are the warning signs of a primary immunodeficency?

A

-multiple infections within the first year
-lack of response to antibiotics
-growth or weight gain delay
-skin, organ abscesses

105
Q

If you are seeing a patient with high levels of bacterial infections, and suspect a immunodeficency, which kind would it be?

A

Humoural, because you would suspect a B-cell disorder

106
Q

If you are seeing a patient with high levels of viral and fungal infections, and suspect a immunodeficency, which kind would it be?

A

A cellular disorder, because you would suspect a T-cell disorder

107
Q

What does SCID stand for?

A

Severe Combined immunodeficiency

108
Q

What is Severe combined immunodeficiency?

A

A group of combined disorders where a person has problems with both T and B cells

109
Q

If there are B-cells present in SCID, what does that mean?

A

If B cells are present in SCID, then they are useless and do not store memory

110
Q

What causes SCID?

A

Genetic mutations cause loss of all immune function->NK cells may still be present though

Most common through X-linked recessive mutation

111
Q

NK cells and T cells are structurally similar, but how are they different?

A

NK cells do not have to be activated through the CD-4 pathway

112
Q

What are the manifestations of SCID?

A

Failure to thrive
Chronic diarrhea
Opportunistic infections (s/sx similar to AIDS)

113
Q

What is the best chance of treatment for SCID? What treatments are promising?

A

A bone marrow transplant is the best chance of treatment within the first few months of life to repopulate immune system

Gene therapy is promising

114
Q

Where is bone marrow taken from?

A

The posterior pelvis

115
Q

Many primary immunodeficency disorders traced to a definicency in __________________ _____________ can be cured by?

A

stem cells

They can be cured with allogenic stem cells transplantation from an unaffected donor

116
Q

How is an allogenic stem cell transplant performed?

A

The bone marrow cells of the host are destroyed by chemo before the transplant.

The transplanted stem cells can repopulate the bone marrow and reestablish hematopoises

117
Q

What are the different types of grafts?

A

Autograft
Allograft
Syngeneic
Xenograpft

118
Q

What is an autograft?

A

A graft within the same person

I.E: Burn grafts

119
Q

What is an Allograft?

A

A graft between different people of the same species

120
Q

What is a Syngenetic graft?

A

Donor and recipient of the graft are identical twins

121
Q

What is a xenograft?

A

A graft between species

122
Q

What must transplants be matched by?

A

Transplants must be matched to donors by HLAs (human leuckocyte antigen complex)

123
Q

The better the _________________ matching decreases the chance of transplant rejection.

A

MHC/HLA

124
Q

What are the subtypes of MHC Class 1?

A

HLA-A
HLA-B
HLA-C

These are present in all nucleated cells

125
Q

What are the subtypes of MHC Class 2?

A

HLA-DR
HLA-DP
HLA-DQ

These are present on most immune cells

126
Q

What is the ideal match for transplants?

A

‘8 point match’

127
Q

What type of ‘rejection’ can occur with allografts?

A

Hyperacute, Acute or Chronic

Called Host vs. Graft Disease

128
Q

What occurs in Host vs. Graft disease?

A

The specific tangible organ and host’s immune system starts attacking organ because it recognizes the graft as foreign

129
Q

In a Hyperacute Rejection, what is the?
Timing:
Type of Reaction:
Cause:

A

Hyperacute rejections
Timing: Immediate
Type: Type 3
Cause: Existing host antibodies to graft

*The host’s immune system has pre-existing antibodies to antigens on grafted tissue, as soon as blood vessels are connected, antibodies will get access to grafted tissue. Upon perfusion, graft immediately becomes ischemic then necrotic

130
Q

In an Acute Antibody Mediated Rejection what is the:
Timing:
Type:
Cause:

A

In an acute antibody mediated rejection the
Timing: Days to weeks
Type: Type 4
Cause: Generation of T cells and antibodies against the graft

*Can be eliminated by antirejection meds

131
Q

In a chronic rejection what is the:
Timing:
Type:
Cause:

A

Timing: Months to years
Type: Unclear
Cause: Immune mediated inflammatory injury normally T-cell and macrophage related and is a sign the organ is failing

132
Q

What is graft vs. Host disease?

A

A transplant/graft has a functional cellular immune component

The receipient/host tissue has antigens foreign to the donor tissue

The recipient/hosts immunity is compromise to the point where it cannot destroy the transplanted cells

133
Q

What are the manifestations normally seen in graft vs. host disease?

A

An itchy irrated rash is seen in soft tissues

The pattern of rash is that it starts on extremities and moves inward

GI/Liver can both suffer inflammation and damage

134
Q

What is self tolerance?

A

The body doesn’t mount an immune response against cells with matching HLAs

HLAs mark the bodies own cells as ‘safe’

135
Q

When does an autoimmune disease occur?

A

When the immune sysem loses ability to recognize its own cells and begins to manufacture auto-antibodies

136
Q

What are the triggers of an autoimmune disease?

A

Viruses
Hereditary
Hormones
Drugs

(estrogens and androgens may be involved)

137
Q

What are some examples of autoimmune diseases?

A

Rheumatoid arthritis
Systemic Lupus
Scleroderma
Type 1 diabetes
Myasthenia gravis
Ulcerative colitis

138
Q

What are the diagnosis criteria for autoimmune disorders?

A

Evidence, Determination, Lack of Cause

-Evidence of an autoimmune reaction
-Determination that immunicological findings are not secondary to other condition
-The lack of other identified causes for the disorder

139
Q

What is rheumatoid arthritis?

A

An slow onset autoimmune disorder associated with articular and extra-articular manifestations

140
Q

What are the systemic manifestations of rheumatoid arthritis?

A

Fatigue
Anorexia
Weight loss
Generalized ache and stiffness

141
Q

What is rheumatoid arthritis characterized by?

A

Ulnar drift (angle of fingers)
Exacerbations and Remissions

142
Q

What are the criteria for diagnosis of rheumatoid arthritis?

A

Morning stiffness at least 1hr and swelling of three or more joints for at least 6 weeks

Swelling of wrist, metacarpophalangeal or proximal interphalangeal joints for 6 or more weeks

Hand XR changes typical of RA

Rheumatoid Nodules

Serum rheumatoid factor

143
Q

What is the definition of immune hypersensitivity?

A

Excessive or inappropriate activation of the immune response that causes the body damage due to immune response and not antigen

144
Q

What is a type 1 hypersensitivity?

A

Allergic Reactions
IgE-mediated
Fast onset

145
Q

What is a type 2 hypersensitivity?

A

Cytotoxic
Antibody mediated

146
Q

What is a type 3 hypersensitivity?

A

Antigen-antibody (immune complexes)

EX: hyperacute transplant reaction

147
Q

What is a type 4 hypersensitivity?

A

Cell mediated, delayed

PPD is example

148
Q

Which hypersensitivity represents the “classic” allergic response, thought to be genetically influences and can have both systemic/anaphylactic reaction in addition to local/atopic rxns?

A

Type 1

149
Q

The inital exposure in a type 1 hypersensitivity activates?

A

IgE

150
Q

What are the two types of cells involved in type 1 reactions?

A

Helper T cells (T1H or T2H)
Mast cells and basophils

151
Q

What do T1H cells do in type 1 hypersensitivities?

A

Stimulate the differentiation of B cells

152
Q

What do T2H cells do in type 2 hypersensitivites?

A

T2H cells are more involved
They direct B lymphocytes to switch class and produce IgE antibodies

153
Q

What are the phases in a Type 1 hypersensitivity reaction?

A

Primary (initial phase)
Secondary (late phase response)

154
Q

What occurs in the primary phase of a type 1 hypersensitivity reaction?

A

-Occurs within 5-30 min of exposure
-Subsides within 60 min
-Mediated by acute mast cell degranulation (histamine is most recognized mediator)

155
Q

What occurs in the secondary phase of a type 2 hypersensitivity reaction?

A

-Occurs within 2-8 hrs of exposure
-Can last for days
-Results from action of lipid mediators and cytokines released

156
Q

What is Atopy?

A

A genetic predisposition to development of immediate, type IgE mediated hypersensitivity reaction

The local reactions usually occurs when offending allergen is confined to site of exposure

157
Q

What are some examples local Atopic conditions?

A

Asthma
Atopic Dermatitis
Allergic rhinitis
Food Allergies

-Often involve high total serum antibodies and allergen specific IgE

158
Q

What is the pathology of Anaphylaxis?

A

A systemic response to the inflammatory mediators released in type 1 hypersensitivity reactions

159
Q

What do histamine, acetylcholine, kinins, leukotrienes, and prostaglandins do during anaphylaxis?

A

They cause vasodilation

160
Q

What do acetylcholine, kinins, leukotrienes, and prostaglandins do during anaphylaxis>

A

Cause bronchoconstriction

161
Q

How fast does anaphylaxis occur and how is it graded?

A

A catastrophic reaction can begin in minutes and is graded on a 1-4 scale

1=minor
4=fatal

162
Q

What are the common causes of anaphylaxis?

A

Insect or bee venom
Medications (penicillin)
Shelfish
Nuts

163
Q

What are the signs and symptoms of anaphylaxis?

A

Vasodilation->swelling, erythema, angioedema, hypotension

Bronchoconstriction->wheezing, hypoemia

164
Q

What is a Type 2 hypersensitivity reaction?

A

A reaction mediated by antibodies IgG or IgM to intrinsic/extrinsic antigens

165
Q

In a type 2 hypersensitivity reaction, what can occur due to antibody binding?

A

Antibody binding may cause dysfunction or death/destruction of targeted cells

Examples: Mismatched blood transfusions
Drug reactions

166
Q

What are the 4 major mechanisms of type 2 hypersensivity?

A

-Complement system destruction of RBC
-Complement system inflammation and tissue injury
-Antibody against TSH receptor increasing thyroid production and release
-Antibody inhibition of neurotransmitter binding

167
Q

Blood Compatibilites: Type A
What are the-
Antibodies in the plasma:
Antigens in RBC:
Blood Types Compatible:

A

Antibodies in the plasma: Anti-B
Antigens in RBC: A antigen
Blood Types Compatible: A. O

168
Q

Blood Compatibilites: Type B
What are the-
Antibodies in the plasma:
Antigens in RBC:
Blood Types Compatible:

A

Antibodies in the plasma: Anti-A
Antigens in RBC: B antigen
Blood Types Compatible: B, O

169
Q

Blood Compatibilites: Type AB
What are the-
Antibodies in the plasma:
Antigens in RBC:
Blood Types Compatible:

A

Antibodies in the plasma: None
Antigens in RBC: A and B antigens
Blood Types Compatible: A, B, AB, O

(universal recipient)

170
Q

Blood Compatibilites: Type O
What are the-
Antibodies in the plasma:
Antigens in RBC:
Blood Types Compatible:

A

Antibodies in the plasma: Anti-A and Anti-B
Antigens in RBC: None
Blood Types Compatible: O

(O is universal donor)

171
Q

What occurs in a type 3 hypersensitivity reaction?

A

Too many antigen-antibody complexes are formed and spread throughout the blood->these insoluble complexes lodge vessel walls->complement cascades are activated and chemotaxis causes an inflammatory response

172
Q

What pathophysiology occurs from too mant antigen-antibody complexes in a type 3 hypersensitivity reaction?

A

When the complexes lodge in the vessel walls and initiate complement cascades and an inflammatory response, the inflammation ultimately causes vessel and tissue injury and tis damage may progress to necrosis

173
Q

What are some examples of a type 3 hypersensitivity response?

A

Glomerulonephritis
SLE
Rheumatoid arthritis

174
Q

What are two types of type 4 hypersensitivity reactions?

A

Both involve sensitizd T cells

Direct type: CD8 cells
Delayed-type (DTH): involves CD4 cells

175
Q

What are some examples of Type 4 hypersensitivity reactions?

A

PPD Test
Contact dermatis
Hypersensitivity pneumonities

176
Q

What are the signs of growth hormone excess in adults?

A

Known as acromegaly
Englargement of small bones of hands and feet
Enlarged facial features
Prone to hypertension and atherosclerosis

177
Q

Where is the thyroid gland?

A

The middle of the neck

178
Q

What are the functional units of the thyroid?

A

Follicles

179
Q

What is T3?

A

Triodothyronine-the active form of hormone

180
Q

What is T4?

A

Thyroxine-the storage molecule

181
Q

What is the makeup of T3 and T4?

A

They have protien-bound and free components

182
Q

What is a common manifestation of thyroid dysfunction?

A

Goiters, Increased in size of thyroid gland that may occur in hypo, hyper and normal thyroid states
and can be toxic or nontoxic

183
Q

When a person has a reduced amount of final, active thyroid hormones (T3/T4) what does this indicate?

A

Hypothroidism

184
Q

What are the factors in congenital hypothyroidism?

A

Develops at birth
Children have intellectual disability

185
Q

What can cause congenitial hypothyroidism?

A

Lack of thyroid glands
Lack of hormone synthesis
Defiecient TSH secretion from anterior pituitary

186
Q

What are the various ways that hypothyroidism can be acquired?

A

-Primary: Can occur from destruction or dysfunction of the thyroid gland ex: Thyroidectomy
-May also occur from a secondary disorder eg. pituitary disfunction
ex: Hashimoto thyroiditis

187
Q

What is a serious complication of acquired hypothyroidism?

A

Myxedema

188
Q

What is Myxedema?

A

The presence of nonpitting mucus type edema in connective tissues

189
Q

What are some signs and symptoms of hypothyroidism?

A

Weakness and fatigue
Dry hair and skin
Puffy face
Decreased GI motility

190
Q

What is a myxedematous coma?

A

The end stage of severe hypothyroidism that is life threatening and can lead to cardiovascular collapse, metabolic disorders, hypothermia

191
Q

High levels of T4, also known as thyrotoxicosis is more commonly known as?

A

Hyperthyroidism

192
Q

What is the most common cause of hyperthyroidism?

A

Graves Disease (an autoimmune disorder)

Other causes can be: multinodular goiters, adenoma, thyroiditis

193
Q

What are the signs and symptoms of Hyperthyroidism?

A

Nervousness, irratability, fatigue
Weight loss
Tachycardia
Palpitations
Excessive sweating
Heat intolerance
****Exophthalmos (abnormal protrusion of eyeballs)

Never Would Toads Ever Play Here

194
Q

What is a thyroid storm?

A

AKA: A thyrotoxic crisis precipitated by stress that requires rapid treatment

195
Q

What is a thyroid storm manifested by?

A

High fever
Tachycardia
Heart Failure
Chest Pain
Severe CNS effects

196
Q

What are adrenal Androgens?

A

‘Sex hormones’
Contribute to growth of pubic hair

197
Q

What are mineralocorticoids?

A

Regulate potassium, sodium and water balance

Aldosterone is key hormone

Regulated by Renin-Angiotensin

198
Q

What are glucocorticoids?

A

Regulated by negative feedback and cortisol is the main hormone

199
Q

What are the metabolic effects of Cortisol?

A

Stimulates glucose production
Promotes protein breakdown
Mobilizes Fatty Acids

200
Q

What are the psychological effects of cortisol?

A

Can lead to psychosis

201
Q

What are the immunologic and inflammatory effects of cortisol?

A

Blocks inflammation
Supresses immune response

202
Q

Describe the Cortisol Feedback loop?

A

Corticotrophin-Releasing hormone is released from the hypothalamus and stimulates the Anterior pituitary to release ACTH.

ACTH stimulates the adrenal cortex to produce cortisol. Cortisol then shuts down release of CRH from Hyopthalmus in a negative feedback loop

203
Q

What is ACTH?

A

Adrenocorticotropic hormone (ACTH) is a tropic hormone produced by the anterior pituitar

204
Q

What varies about the cortisol feedback loop?

A

It has diurnal variation (peaking in the morning)

Also varies and is impacted by stress

205
Q

What is cushing syndrome?

A

Glucococorticoid hormone excess

206
Q

What forms of Cushing’s syndrome are there?

A

Pituitary Form
Adrenal Form
Etopic Cushing syndrome

207
Q

What are the clinical manifestations of Cushing Syndrome?

A

Altered fat metabolism (Moon face and buffalo hump)
Muscle weakness
Purple Striae
Osteoporosis
Hirsutism (excess hair growth)
Emotional lability

A moon faced hairy man with purple stripes, weak bones is emotional because his muscles are weak.

208
Q

What are the steps for diagnosis and treatment of Cushing Syndrome?

A

Two steps for diagnosis:
Determining increased secretion of cortisol
Finding the cause

Treated by removing or correcting the source of the elevated cortisol levels because it can lead to severe morbidity or death if left untreated

209
Q

What are the hromones of the Adrenal Medulla?

A

Cateocholamines: Norepinephrine and epinephrine, dopamine

210
Q

What does the response to cateocholamines depend on?

A

The type of receptor that is activated (Alpha 1 & 2, Beta 1 & 2)

211
Q

What is a Pheochromocytoma?

A

A catecholamine-secreting tumor of the adrenal medulla that results in catecholamine excess

212
Q

What are the symptoms of Pheochromocytomas?

A

Hypertension
Tachycardia
Palpitations
Diaphoresis
Flushing
N/V
Blurry Vision
Headaches
Hyperglycemia

213
Q

What is thirst controlled by?

A

The hypothalamus

214
Q

What stimulates thirst?

A

Cellular dehydration or decrease in overall ECF

215
Q

What is a decreased ability to sense thirst?

A

Hypodipsia

216
Q

What is an increased thirst that is abnormal and results in excessive water intake?

A

Polydipsia

217
Q

What is ADH?

A

A hormone that is secreted by the posterior pituitary and controls reabsorption of water by the kidneys by acting on vasopressin receptors in the kidney which causes increased water reabsorption and decreased urine volume

218
Q

What effects the production of ADH?

A

ECF volume and osmolality

219
Q

What is diabetes insipidus?

A

A deficiency of ADH or reduced response of the kidneys to ADH and results in the inability to concentrate urine

220
Q

What are the signs and symptons of Diabetes insipidus?

A

Polyuria
Polydipsia
Possibly FVD is cannot access enough fluids

221
Q

What is SIADH?

A

Syndrome of inappropriate ADH where ADH is released even though serum osmolality is decreased and results in water retention and dilutional hypoatermia

222
Q

What are the signs and symptoms of SIADH?

A

Water rention and dilutional hypoatremia

NURS 709 Pathophysiology (5 decks)

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