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Pathology > Block 11 > Flashcards

Block 11 Flashcards

1
Q

What is leukemia

A

Cancer of the WBCs/blood/bone marrow

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2
Q

What is leukocytosis

A

Increase in the total WBC count

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3
Q

What is neutrophilia

A

Increase in the neutrophil count

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4
Q

What is lymphocytosis

A

Increase in lymphocyte count

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5
Q

What is leukopenia

A

Decrease in the total leukocyte count

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6
Q

What is neutropenia

A

Decrease in neutrophil count

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7
Q

Lymphocytopenia

A

Decrease in lymphocyte count

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8
Q

What is pancytopenia

A

All blood lineages are decreased

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9
Q

What is the leukemoid reaction

A 
Leukemia like infection 
Neutrophils increase (
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10
Q

T/F leukemoid reaction is a form of leukemia

A

False

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11
Q

What is leukemoid reaction often confuse with

A

Chronic myelocytic leukemia

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12
Q

Who is acute lymphocytic leukemia most common in

A

Children (3-7 yoa)

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13
Q

What are the symptoms of ALL

A 
Acute illness
Pale
Bruises easily
Bleeding gums
Infection
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14
Q

What is seen in labs of ALL patients

A

WBC very low or very high

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15
Q

What is diagnostic of ALL

A

Tdt

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16
Q

What is the prognosis for people diagnosed with ALL

A

Good prognosis

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17
Q

Who is most commonly affected with Acute myeloid leukemia (AML)

A

Adults (approx 55 yoa)

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18
Q

What are the symptoms of AML

A 
Acute illness
Pale
Bruises easily
Bleeding gums
Infection
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19
Q

What is seen in labs for AML

A

> 20% blasts in bone marrow

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20
Q

What is diagnostic of AML

A

Auer rods

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21
Q

What is the prognosis of AML

A

Poor prognosis

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22
Q

Who is most commonly affected by chronic myeloid leukemia (CML)

A

Adults (age 50)

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23
Q

What are the symptoms of CML

A

They are usually asymptomatic

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24
Q

What is usually seen in labs for CML patients

A

High WBCs

Immature/mature neutrophils

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25
Q

What is diagnostic of CML

A

Philadelphia chromosome

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26
Q

What drug has been used and increased the survival of CML

A

Gleevec

>80% remission

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27
Q

What is the most common leukemia

A

Chronic lymphocytic leukemia (CLL)

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28
Q

Who is usually affected by CLL

A

Adults (>50 yoa)

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29
Q

What is seen in labs for CLL

A

Increase WBCs (>20K)

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30
Q

How is CLL found

A

Usually found by accident at a physical

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31
Q

What is the survival of CLL

A

10 year survival for types 1 and 2

<2 year survival for types 3 and 4

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32
Q

T/F you probably wont kill CLL

A

True

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33
Q

How do you treat CLL

A

You normally don’t treat it

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34
Q

What is diagnostic of Hodgkins Lymphoma

A

Reed-Sternberg cells

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35
Q

What is the survival of Hodgkins Lymphoma

A

85% survival

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36
Q

What is non-Hodgkins Lymphoma survival

A

69% survival

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37
Q

What is Lymphoma stage 1

A

Single lymph node affected

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38
Q

What is lymphoma type 2

A

2 or more lymph nodes on one side of diaphragm

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39
Q

What is lymphoma type 3

A

Cancer spreads to both sides of diaphragm or involves spleen

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40
Q

What is lymphoma stage 4

A

Liver, bone marrow, lung

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41
Q

What is the hemoglobin rule of 3

A

Hemoglobin x3= hematocrit +/-3

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42
Q

How do you find hemoglobin from hematocrit

A

Hematocrit /3 : hemoglobin

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43
Q

What is the size of RBC comparable to

A

The size of lymphocytic nucleus

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44
Q

What is anemia

A

HGB and HCT are both low

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45
Q

What are the 3 causes of anemia

A

Blood loss
Impaired RBC production
Accelerated RBC destruction

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46
Q

What is hypochromic

A

Low MCHC

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47
Q

What is hyperchromic

A

High MCHC

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48
Q

What is microcytic anemia

A

MCV<75

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49
Q

What are the 1st and 2nd most common of microcytic anemia

A
  1. Iron deficiency

2. Thalassemia

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50
Q

What is normacytic anemia

A

MCV 80-98

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51
Q

What is macrocytic anemia

A

MCV>100 `

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52
Q

What are the common forms of macrocytic anemia

A

B12/folate deficiency

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53
Q

How much B12 is stored

A

3 years worth

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54
Q

How much folate is stored

A

3 months

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55
Q

What vegetable can cause hemolytic anemia

A

Fava beans

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56
Q

What drugs can cause hemolytic anemia

A

NSAIDs
Sulfa drugs
Anti-malarial drugs

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57
Q

What is hemolytic anemia associated with

A

G6PD deficiency

Sickle cell anemia

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58
Q

What does G6PD and sickle cell anemia protect against

A

Malaria

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59
Q

Where is thalassemia common

A

Mediterranean (Italy/Greece)

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60
Q

What is thalassemia confused with

A

Microcytic hypochromic anemia

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61
Q

How does thalessemia appear for RDW

A

Normal

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62
Q

The conducting unit of the respiratory system

A 
Nasal cavity
Nasopharynx
Larynx
Trachea
Bronchi
Bronchioles
Terminal bronchioles
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63
Q

What is the respiratory unit of the respiratory system

A

Respiratory bronchioles
Alveolrar ducts
Alveoli

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64
Q

What is obstructive

A

Airway conduction is compromised (bronchitis, asthma

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65
Q

What is restrictive

A

Lung expansion is compromised (fibrosis)

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66
Q

Sinusitis

A

Inflammation of the mucous membranes of the paranasal sinuses

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67
Q

Sinusitis in adults

A

Maxillary sinus

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68
Q

Sinusitis in children

A

Ethmoid sinus

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69
Q

What are som causes of sinusitis

A

Upper respiratory infection (bacterial or viral)

Deviated nasal septum
Smoking

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70
Q

What pathogen is mostly associated with sinusitis

A

Streptococcus pneumoniae

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71
Q

What are the symptoms of sinusitis

A

Pain over sinus
Nasal congestion
Fever
Cough

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72
Q

How do you diagnose sinusitis

A

X ray

CT

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73
Q

T/F sinusitis can affect the eye

A

True

It can spread to the orbit and cause sinusitis

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74
Q

What is laryngitis

A

Inflammation of the larynx

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75
Q

What is a common cause of laryngitis

A

Viral (most common) or bacterial

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76
Q

What are the symptoms of laryngitis

A

Coarse voice
Fever
Heals within days

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77
Q

What are 2 important types of laryngitis

A

Croup

And diphtheria

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78
Q

What is croup

A

Barking cough

Children

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79
Q

What is diphtheria

A

Rare
Suffocation
Death

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80
Q

What is pharyngitis?
Symptoms?
Test?

A

Strep threat
With pain, adenopathy, NO cough

Rapid Strep test

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81
Q

What is tracheitis and bronchitis?

A

Inflammation of the trachea and he bronchi

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82
Q

What is pneumonia

A

Inflammation of the lungs

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83
Q

What is typical pneumonia caused by?

A

Bacterial

Streptococcus pneumoniae

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84
Q

What is bronchopneumonia

A

Begins as acute bronchitis and spreads to the lungs

The lower lobes or right middle lobe is usually affected

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85
Q

What is lobar pneumonia

What are the complications?

A

Complete consolidation of a lobe of the lung

Lung abscess, emphysema, sepsis

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86
Q

What are the clinical findings of pneumonia

A

Sudden onset of high fever
Productive cough
Chest pain
Tachycardia

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87
Q

How do you diagnose pneumonia

A

Chest X-ray

Lab tests

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88
Q

What is atypical pneumonia?

What causes it

A

In young individuals

Mycoplasma pneumoniae (viruses_

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89
Q

What are the clinical findings of atypical pneumonia

A 
Asking pneumonia 
Low grade fever
Nonproductive cough
Chest pain
Flu-like symptoms
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90
Q

What is tuberculosis caused by

A

Inhalation of mycobacterium tuberculosis

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91
Q

Where does the Bacteria for TB reside

A

In the phagosomes of alveolar macrophages

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92
Q

How do you screen for TB

A

PPD skin test

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93
Q

What is primary TB`

A 
Can be symptomatic or asymptomatic
Upper part of lower lobe
Lower part of upper lobe
Caseus necrosis in periphery and hilar lymph nodes 
Usually resolves
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94
Q

What s secondary TB

A

Reactivation of previous TB infection

Cytokines from memory T cells released
Severe
Can spread out of lungs

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95
Q

What are the clinical findings of TB

A

Fever
Drenching night sweats
Weight loss

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96
Q

What are the complications of TB

A

Can spread in lungs, can spread out of lungs
Kidneys can be affected
Spread to vertebrae, meninges, etc

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97
Q

What does introcular TB usually infect

A

Uveal tract

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98
Q

Anterior intraocular TB

A

Granulmatous keratic precipitates

Iris granulomas
Cataracts

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99
Q

Posterior intraocular TB

A

Most common

Can mimic tumor

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100
Q

Retinal TB

A

Uncommon
Exudative hemorrhagic lesions
Scars can form

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101
Q

TB of external eye

A

Affects orbit, eyelid, lacrimal gland, conjunctiva, sclera

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102
Q

What is influenza caused by

A

Influenza virus A and B

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103
Q

What can complicate influenza infection

A

Staphylococcus aureus

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104
Q

What are the symptoms of influenza

A

High fever, joint pain, malaise, pain with eye movements

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105
Q

Antigen drift:

A

Mild mutation, no new vaccine needed

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106
Q

Antigen shift:

A

Major mutation, new vaccine needed

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107
Q

What is COPD?
Common cause?
2 conditions?

A

Progressive irreversible obstruction of airflow out of the lungs

Smoking

Emphysema and chronic bronchitis

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108
Q

What is emphysema

A

Enlargement of all or part of the respiratory unit

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109
Q

What is the most common cause of emphysema?

A

Smoking

AAT deficiency

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110
Q

What is the pathogenisis of emphysema

A 
Increase compliance
Decreased elasticity 
Destruction of elastic tissue
Loss of radio traction
Small airways collapse on expiration
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111
Q

What is chronic bronchitis

Common cause?

A

Productive cough that lasts for 3 months for 2 years

Smoking

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112
Q

What is the pathogenesis of chronic bronchitis

A

Hyper-secretion of mucus in the bronchi
Obstruction of the airlift
Irreversible fibrosis

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113
Q

What are the clinical findings of the chronic bronchitis

A

Productive cough
Dispnea
Hypoemia

Large horizontally oriented heart

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114
Q

What is bronchial asthma

A

Epidemic reversible disease of the bronchi

Thick bronchial basement membrane

Dyspnea with episodic expiratory wheezing
Nocturnal cough

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115
Q

What is asthma

A

Type 1 HS rxn to extrinsic allergens
Runs in families

Initial: CD4, IL4
2nd exposure: IgE, release histamine,
Bronchoconstriction, mucus production, influx of leukocytes

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116
Q

What is the most common cardiovascular cause of death after acute myocardial infarction and stroke

A

Pulmonary thromboembolism

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117
Q

Where do the majority of pulmonary thromboemboli originate from

A

Deep veins of the lower extremities and pelvis

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118
Q

What are the risk factors for PE

A 
Prolonged bed rest
Hypercoagulable states (dense blood)
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119
Q

Large emboli occlude….

A

Main pulmonary arteries

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120
Q

Small emboli occlude….

A

Medium-sized and small pulmonary arteries

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121
Q

What are the consequences of pulmonary artery occlusion

A
  • Increase in pulmonary artery pressure
  • decrease blood flow to pulmonary parenchyma
  • hemorrhagic infarction
  • perfusion is greater than ventilation in the lower lobes
  • majority are located in the lower lobes
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122
Q

What are the clinical findings of PE

A 
Saddle embolus: sudden death
Sudden onset of dyspnea and tachypnea 
Pleuritic chest pain
Fever
Expiratory wheezing
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123
Q

How do you diagnose PE

A

Spiral CT
Abnormal perfusion radionuclide scan
Positive d-dimers-non-specific

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124
Q

What is pulmonary hypertension?

A

Mean PAP>25 mmHG at rest

Mean PAP>30 mmHG with exercise

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125
Q

What is primary PH

A

Cause is not known
More common in women
Genetic predisposition

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126
Q

What is secondary PH

A

Comorbid condition causes the HTN

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127
Q

What are the 2 ways that secondary PH occurs

A
  1. Endothelial cell dysfunction, loss of vasodilator, increase in vasoconstrictors
  2. Hypoxemia and respiratory acidosis stimulate vasoconstriction of pulmonary arteries , smooth muscle hypertrophic and hyperplasia
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128
Q

What is for pulmonale

A

Combination of PH and RVH leading to right sided heart failure

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129
Q

What are some causes of Cor pulmonale

A 
Chronic hypoxemia
Chronic respiratory acidosis
Chronic bronchitis
Emphysema
Volume overloading pulmonary vasculature 
Left sided vasculature disease
Backup of blood into pulmonary veins
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130
Q

What are teh pathologic findings with Cor pulmonale

A

Atherosclerosis of main elastic pulmonary arteries smooth muscle hypertrophy

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131
Q

What is pulmonary edema

A

Excess fluid in the lungs

Fluid collects in the air sacs and makes it difficult to breathe

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132
Q

What usually causes pulmonary edema

A

Heart problems

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133
Q

What are the 2 mechanisms of pulmonary edema

A
  1. Increased hydrostatic pressure in lung capillaries
    - left sided heart failure, volume overload, mitral stenosis
  2. Decreased oncotic pressure
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134
Q

What are some things that can cause pulmonary edema

A

Infections
Aspiration
Drugs
High altitude

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135
Q

What is chronic interstitial lung disease

A

Fibrosing disorders

Granulomatous disease

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136
Q

What is the pathogenesis of interstitial fibrosis

A

Early: alveolitis

Leukocytes release cytokines, that stimulate fibrosis

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137
Q

What are the effects of interstitial fibrosis

A

Decreases lung compliance (decreased expansion)

Increases lung elasticity (stiffness)

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138
Q

What are the clinical findings of interstitial lung disease

A

Dry cough
Exerting dyspnea
Potential for Cor pulmonale

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139
Q

Who is most affected by idiopathic pulmonary fibrosis

A

Smoking males

40-70 yoa

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140
Q

What is the pathogenesis of idiopathic pulmonary fibrosis

A

Repeated alveolitis
Release of cytokines produces interstitial fibrosis
Proximal dilation of small airways
Lung has honey comb appearance

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141
Q

How does the Lung appear in idiopathic pulmonary fibrosis

A

Honeycomb

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142
Q

What are the clinical findings of idiopathic pulmonary fibrosis

A

Fever
Progressing dyspnea with exertion
Chronic nonproductive cough
Late inspiratory cackle

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143
Q

What is pneumoconioses

A

Inhalation of mineral dust not the lungs leading to interstitial fibrosis

Mineral dust includes coal dust, silica, asbestos, and beryllium

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144
Q

Particles >5um are captured by

A

Large bronchi and eliminated by coughing

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145
Q

Particles >0.5um…

A

Reach the alveoli and are phagocytosed by alveolar macrophages

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146
Q

Particles 1-5 um…

A

Get stuck at the bifurcation or bronchioles/alveolar ducts

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147
Q

What is the least fibrogenetic particle

A

Coal dust

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148
Q

What substances are very fibrogenic

A

Silica
Asbestos
Beryllium

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149
Q

What is anthracosis

A

Coal workers pneumoconiosis

Usually asymptomatic
Pigment in interstitial tissue and hilar nodes

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150
Q

What is simple coal workers pneumoconiosis

A

Fibrotic opacities are smaller than 1 cm in upper lobes and upper portions of lower lobes

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151
Q

What is complicated wool workers pneumoconiosis

A

Fibrotic opacities larger than 1-2cm IR without necrotic centers

Crippling lung disease (black lung)

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152
Q

What is sarcoidosis

A

Multi-system noninfectious granulomatous disease that produces chronic interstitial fibrosis

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153
Q

Who is affected most commonly by sarcoidosis

A

Black
Non smokers
Women
20-39 years old

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154
Q

What is the pathogenesis of sarcoidosis

A

Disorder in immune regulation

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155
Q

What must you rule out when diagnosing sarcoidosis

A

Granulomatous disease

156
Q

What is the primary target of sarcoidosis

A

Lung

157
Q

What is the most common symptom of sarcoidosis

A

Dyspnea

158
Q

What are the skin lesions with sarcoidosis

A

Modular lesions containing granulomas

159
Q

What are eye lesions with sarcoidosis

A

Uveitis

160
Q

What s seen in lab tests for sarcoidosis

A

Increase ACE

161
Q

How is sarcoidosis treated

A

It is not really treated unless required (steroids)

It usually resolves on its own in 3 years

162
Q

What is the most common fatal cancer in both mean and women worldwide

A

Primary lung cancer

163
Q

What are some causes of lung cancer

A 
Smoking
Risk increases with quantity and duration of smoking
Men have a greater risk 
Asbestos
Certain metals
Secondhand smoke
164
Q

What are some classification of primary lung cancer?

A 
Adenocarcinoma 
Squamous cell carcinoma 
Small cell lung carcinoma 
Large cell carcinoma 
Bronchial carcinoid

Small cell and non-small cell

165
Q

What is small cell lung cancer prognosis

A

Very malignant

166
Q

What is non-small cell carcinoma prognosis

A

Better

Longer life expectancy

167
Q

Where are the common sites for metastasis

A 
Hilar lymph nodes * most common 
Adrenal gland
Liver
Brain
Bone
168
Q

What are teh molecular genetics of lung cancer

A

Gene mutations

Oncogenes (promote cell survival and division)
Suppression genes (promote cell apoptosis) p53
169
Q

What are the clinical findings in primary lunch cancer

A 
Cough
Weight loss
Hemoptysis
Dyspnea 
Chest pain
170
Q

What is adenocarcinoma

A

Peripheral tumor
Most common
In non-smokers, women

Grows slowly but metastasizes early

Scar carcinoma develop in scars

171
Q

What is squamous cell carcinoma

A

Central
More common in men
Strong association with smoking
P52 mutations

172
Q

What is pancoast tumor

A

Lung carcinoma in the apex o lungs

173
Q

What Can a pancoast tumor cause

A

Horners syndrome

174
Q

What is the triad of Horner’s syndrome

A

Ptosis
Mitosis
Anhidrosis

Compression of the superior sympathetic ganglia

175
Q

What is pneumothorax

A

Air in thoracic cavity

176
Q

What is hemothorax

A

Blood in thoracic cavity

177
Q

What is atelectasis

A

Loss of lung volume caused by collapse of alveoli

Results in shunting of inadequate oxygenated blood from pulmonary arteries to veins

178
Q

What is disruptive sleep apnea

A

Excessive snoring with intervals of breath cessation

179
Q

What are some causes of sleep apnea

A

Obesity (the pharyngeal muscles collapse)

180
Q

What is the pathogenesis of sleep apnea

A

Airway obstruction causes CO2 retention and hypoxemia

181
Q

What is the cardiovascular systems job

A

To maintain sufficient blood pressure to profuse the body

182
Q

T/F the body will alter Hr, contractility, and vessel diameter, CO, peripheral resistance and blood volume to maintain MAP

A

True

183
Q

What is teh leading cause of death in the US

A

Cardiovascular disease

184
Q

What are the most common CVDs?

A

Hypertension

Coronary artery disease

185
Q

What doe CVD risks increases with

A

Age and lifestyle choices

186
Q

What is high BP

A

14-/90

187
Q

What is normal BP

A

120/80

188
Q

What is primary HTN

A

Don’t know the cause

189
Q

What is secondary HTN

A

Due to another disease/drug

Can resolve with cause

190
Q

What can prolonged HTN cause

A

Damage to vessel walls

Arteriosclerosis, atherosclerosis, stroke, CAD

191
Q

What are the risk factors of HTN

A

Cardiac hypertrophy
Heart failure
Retinal exudates
Flame and hemorrhages

192
Q

What does injury to vessel wall cause

A

Remodeling

It is normal with aging

193
Q

What can excessive vessel remodeling lead to

A

Arteriosclerosis

Atherosclerosis

194
Q

What is hyaline arteriosclerosis

A

Aging process accelerated by hypertension
In less sever HTN
Increased ECM narrows artery ad reduces compliance

195
Q

What is hyperplastic arteriosclerosis

A

In severe HTN
New smooth muscle cells (onion)
Narrows vessel, reduces compliance and causes vessel necrosis

196
Q

What is atherosclerosis

A

Prescence of plaques in arteries
Weakens the vessel
If it ruptures it can cause a clot
Clot can break off and lodge elsewhere

197
Q

What are some of the treatments for HTN

A 
Lifestyle changes
BB, CCB
Diuretics
ACEI, ARBs
Cholesterol lowering medications
198
Q

What are some causes of heart disease

A 
Failure of pump
Obstruction of flow
Regurgitant flow
Flow disorders
Conduction disorders
199
Q

When do pump failures occur

A

When the heart cannot maintain cardiac output or can only maintain it at altered filling pressures

200
Q

What is systolic heart failure

A

Heart cannot generate sufficient force

Due to ischemia or HTN

201
Q

What is diastolic heart failure

A

Heart cannot properly relax

Due to HTN, fibrosis, or pericarditis

202
Q

What is myocardial ischemia

A

A heart attack

Lack of sufficient blood flow to the heart

203
Q

What can cause a MI

A

Reduced blood flow to overworked muscle

Clot in the coronary circulation

204
Q

What is the result of MI

A

Loss of heart muscle and production of non-contractile scar

205
Q

What usually proceeds heart failure

A

Periods of angina, dyspnea, and confusion

As heart muscle dies, biomarkers are released and can be examined

206
Q

What is the only treatment for MI

A

Restore blood flow by stent or bypass

207
Q

What is left sided heart failure

A

The left ventricle is the cause of failure

The left side cant pump what the right side gives it, so volume builds up in the lung

Increased volume increases pressure and causes pulmonary edema

Increases workload on the heart

208
Q

What is right sided heart failure

A

The right ventricle is the cause

Right side cant pump what the left gives it, volume builds up the periphery

Edema in the liver and legs

Increases workload on the left side

209
Q

How do you treat heart failure

A

Reduce workload of heart (B.B., CCB, diuretics)

Increase contractility to increase CO nad maintain fxn (B Ag, cardiac glycosides)

Heart transplant in only cure

210
Q

What are some things that cause flow abnormalities

A

Flow obstruction
Regurgitant flow
Disordered flow

211
Q

What is an obstructive flow

A

Stenotic valves of hypertension increase pressure required to move blood

Can lead to hypertrophy and fibrosis

212
Q

What is regurgitant flow

A

Valves do not close properly, increase volume moving backwards

Leads to dilation of the heart

213
Q

What is disordered flow

A

Vessel abnormalities reduce flow to the periphery

Aneurysms, coarted arota, patent ductus arteriosis

214
Q

What is the treatment for Flow abnormalities

A

Fix the reason for altered flow

Surgery
Replace old valves
Have to be replaced every couple of decades

215
Q

What are som conduction abnormalities

A

Arrhythmia

216
Q

What is an arrhythmia

A

Damage to the conduction system of the heart that causes altered conduction pathways and irregular heart beats

217
Q

What is the most dangerous arrhythmia

A

Ventricular arrythmia

218
Q

What is the most common arrythmia

A

Atrial fibrillation

219
Q

What is atrial fibrillation

A

Non-contracting atria

Has little affect on the heart
Atria only matter at high heart rates or in late heart failure

Causes pooling of blood, clots can form on walls

220
Q

What must you pull all afib patients on

A

Anti-coagulant

221
Q

What are some examples of endocrine disorders

A 
Diabetes
Thyroid diseases
Parathyroid diseases
Pituitary disorders
Adrenal dysfunctions
222
Q

What is insulin released by

A

B cells of the pancreas

223
Q

What is insulin made up of

A

A,B,C chains

The C chain is removed during production and secreted with insulin

224
Q

How is insulin secretion regulated

A
  1. Insulin is secreted when blood glucose is high
  2. GLUT2 transports glucose into B cells
  3. Glucose is oxidized to produce ATP
  4. high ATP levels cause closure of ATP sensitive K channels
  5. Less K leaving the cell causes depolarization
  6. Depolarization opens Ca channels
  7. Ca causes exocytosis of insulin into the blood stream
225
Q

What is the MOA of insulin

A

Binds its receptor (receptor tyrosine kinase)

Receptors phosphorylate themselves and become active

They phosphorylate other proteins inside the cell (IRS-1 and GLUT 4)

Receptor is then internalized and destroyed/recycled

226
Q

What are the major actions of insulin

A
  • storage of excess energy
  • decrease blood glucose levels
  • decreases blood fat levels
  • decreases blood A.A levels
227
Q

What is diabetes mellitus

A

Group of diseases with a common presentation of hyperglycemia

228
Q

What is normal fasting glucose

A

70-100

229
Q

What is pre-diabetic glucose levels

A

100-125

230
Q

What is diabetes glucose levels

A

<125

231
Q

What is insulin dependents diabetes

A

10%
Type 1/juvenile
Autoimmune destruction of B cells

-no insulin is produced
-increases blood levels of glucose, lipids, and proteins
Muscle wasting
Diabetic ketoacidosis due to use of fats as energy. Diuresis, acidosis, hyperkalemia

232
Q

What is the treatment for insulin dependent diabetes

A

Lifelong insulin therapy

233
Q

What is non insulin dependent diabetes

A

90%
Type 2/adult onset
Loss of insulin sensitivity due to chronic high levels of BG

Make insulin but we don’t respond to it

234
Q

What are the treatments for non-insulin dependent diabetes

A 
Life style changes
Metformin
Sulfonylureas
Thiazolidinedione
SGLT2 inhibitors
235
Q

What is the HPT axis

A

Production of T3/T4
Hypothalamus releases TRH
Ant. Pit releases TSH
Thyroid releases T4 and T3

236
Q

What thyroid hormone is more potent

A

T3

237
Q

What thyroid hormone is more produced

A

T4

238
Q

What makes T3/T4 master metabolic hormones

A

Signals through a steroid pathway

Bone growth and maturation

CNS maturation
Increases BMR and heat production
Increases all body metabolisms
Increases cardiac output

239
Q

How does T3/T4 work

A

It’s a peptide hormone that acts like a steroid

Intracellular receptor
Directly initiates transcriptional changes

240
Q

What is hyperthyroidism

A

Too much T/3T4 (Graves)

241
Q

What are the symptoms of Graves

A 
Weight loss 
Increased appetite
Heat intolerance
Sweating
Increased cardiac output
Exopthalmos
Goiter
242
Q

How is graves diagnosed

A

Serum TSH and T/T4 levels

243
Q

What is the treatment for hyperthyroidism

A

Remove thyroid/tumor

244
Q

What is hypothyroidism

A

Not enough T3/T4

Hashimotos
Iodine deficiency
Ceongenital

245
Q

What are the symptoms of hypothyroidism

A 
Weight gain
Cold intolerance
Low cardiac output
Mental slowness
Lack of energy
Myxedema(swollen puffy skin)
246
Q

How do you diagnose myxedema

A

Serum TSH

247
Q

How do you treat hypothyroidism

A

Give them exogenous T3/T4 or iodine

248
Q

What is ceongental

A

Cretinism

T3/T4 is needed for development

Physical and mental develop abnormalities

Learning disabilities
Growth inhibited
Protruding tongue
Umbilical hernia

249
Q

What is Hashimoto’s thyroiditis

A

Autoimmune destruction of the thyroid gland

Old women

First sign is goiter
Anti-thyroid antibodies
Inflammation and cell death in the thyroid

250
Q

What is a goiter

A

Enlarged thyroid
Caused by low iodine
Can occur in hyper/hypothyroidism

Can lead to thyroid tumors

251
Q

What do the parathyroid glands release

A

PTH from chief cells

252
Q

What does PTH respond to

A

Serum ionized calcium levels
Released in repsonse to low levels

Works to raise blood calcium levels

253
Q

What are the actions of PTH

A

Works on kidney to increase phosphate excretion and calcium reabsorption

  • increase osteoclasts activity
  • activates VitD to allow for better absorption of dietary Calcium
254
Q

What is primary hyperparathyroidism

A

Due to parathyroid tumor

255
Q

What are the symptoms of primary hyperparathyroidism

A 
Hypercalcemia
Weakened bones
Hypophosphatemia
Renal stones block ureter 
Constipation
Depression
256
Q

How do you treat primary parahyperthyroidism

A

Remove tumor

257
Q

What is secondary hyperparathyroidism

A

Due to renal failure
VitD must be activated in the kidney

Hypocalcemia due to dietary absorption which increases PTH levels

Bones are dissolved and serum calcium is restored

Weakened bones
Possible calcifications of some vessels

258
Q

What is hypoparathyroidism

A

A rare condition
Due to thyroid removal
Congenital abnormality
Autoimmune destruction of parathyroid glands

259
Q

What are the symptoms of hypoparathyroidism

A 
Hypocalcemia
Hyperphosphatemia
Muscle spasms
Tetany
Cardiac arrhythmias
Increases intracranial pressure 
Seizures
Clotting disorder
260
Q

What does the anterior pituitary release a lot of

A

Stimulating hormones

And GH’s

261
Q

What is hypopituitarism due to

A

Non functioning tumor
Congenital
Ischemia
Radiation damage

262
Q

What can hypopituitarism result in

A

Slow loss of most downstream glandular function

FSH/LH lost first
GH 2nd lost
Thyroid/ACTH last to go

263
Q

What is hyperpituitarism due to

A

Tumor in pituitary gland

264
Q

What are the tumors in hyperpituitarism composed of

A

One cell type

Will produce too much of only one hormone

265
Q

T/F GH doesn’t have a downstream gland

A

True, its special

266
Q

What is the MOA of growth hormone

A

-GH binds receptor and causes phosphorylation of intracellular proteins
-regulates blood levels of all energy sources
-causes protein synthesis and organ growth
-linear bone growth
=produces somatomedins that act like GH in some targets

267
Q

What causes GH deficiency

A

Pituitary damage

268
Q

What occurs in GH deficiency in Newborns (congenital)

A

Failure to grow and develop normally in first months

Must give GH to allow catchup

269
Q

What occurs in GH deficiency in children (acquired)

A 
Short (dwarfism if not corrected)
Under developed
Poor bone density
Low muscle mass
Late puberty
270
Q

What occurs in GH deficiency in Adults (acquired)

A

Loss of lean muscle
Obesity
Poor bone density
Increased risk of cardiovascular disease

271
Q

What normally causes GH excess

A

Tumor

272
Q

What occurs in GH excess in newborns and children

A
  • Pituitary gigantism
  • Rare
  • Increased linear growth
  • early mortality due to overgrowth of organs
  • predisposition to diabetes, HTN, osteoporosis
273
Q

What occurs in GH excess in adults

A 
Acromegaly
Due to pituitary tumor
Growth of all soft tissues and organs
Cardiovascular issues
Long fingers
No gain in height
Insulin resistance
Peripheral vision loss
274
Q

What do the adrenal glands produce

A

Glucocorticoids
NE
Epi
mineralcorticoids (aldosterone)

275
Q

What is cortisol

A

Stress hormone

276
Q

What affects does cortisol have

A
  • Increases protein catabolism
  • increase fatty acid usage
  • maintenance of blood glucose levels
  • stimulates gluconeogensis by liver
  • anti-inflammatory and immunosuppression
277
Q

What is hypercortisolism usually caused by

A

Taking Glucocorticoids

Too much ACTH or adrenal tumor

278
Q

What us Hypercortisolism (Cushings)

A 
Adrenal produces too much cortisol 
Hyperglycemia
Weight gain
Central obesity 
Moon face
Buffalo hump
Muscle wasting
HTN
Virilization
279
Q

What is hypocortisolism due to

A

Autoimmune destruction of adrenal cortex (common after TB)

280
Q

What are the symptoms and causes of Hypocortisolism (Addison’s)

A

Adrenal don’t make enough cortical hormones

Hypoglycemia
Weight loss
Muscle weakness
Hypotension
Hyperkalemia
Metabolic acidosis
Hyperpigmentation
281
Q

What causes hyperpigmentation in Addison’s

A

Overproduction of ACTH
ACTH and MSH come from the are protein

Bronze skin and dark organs

282
Q

What is pheochromocytoma

A

Tumors of chromaffin cells
Common symptom of HTN

Diagnose by imaging serum Epi/NE

Treat by removing the tumor

283
Q

What is achalasia

A

Incomplete relaxation of the lower esophageal sphincter in response to swallowing

284
Q

What is the physiological sphincter of the esophagus

A

Lower sphincter

285
Q

What is primary achalasia

A

Mesenteric ganglia that carry the vagal fibers from the esophagus are absent

286
Q

What is the danger of achalasia

A

Aspiration of esophageal content into the lungs

287
Q

What can the stasis of food sue to achalasia cause

A

Inflammation or ulceration

288
Q

What is a hiatal hernia

A

Herniation of the stomach through the esophageal hiatus of the diaphragm

289
Q

What is GERD

A

Reflux or backward movement of gastric contents into the esophagus

290
Q

What are some presentation of GERD

A

Heartburn or pyrosis associated with eating

291
Q

What causes GERD

A

Weak or incompetent lower esophageal sphincter causes GERD

292
Q

What are some agents that decrease the one of the esophageal sphincter

A 
Food
CNS depressants
Obesity
Preggo
Hiatal hernia
Delayed gastric emptying
Increased gastric volume
293
Q

How do you treat GERD

A 
Avoid positions that cause reflux
Avoid large meals
Avoid trigger foods
Weight loss
Drugs (antacids, etc.)
294
Q

What are the symptoms of GERD

A

Heart burn 30-60 min after eating that is relieved by sitting upright

Wheezing, chronic cough, hoarseness of voice

295
Q

What is GERD often confused with

A

Angina

296
Q

Where is the pain with GERD

A

Epigastric or retrosterna area that radiates to the throat, shoulder, or back

297
Q

What is Barrett’s esophagus

A

Distal esophageal squamous cells replace columnar epithelium containing goblet cells

A complication of GERD

The inflammation leads to ulceration

298
Q

What are the complications of Barrett’s esophagus

A

Strictures and ulcers

299
Q

Why can Barrett’s esophagus form adeocarcinoma

A

30-40%
Because of high grade dysplasia

Needs periodic screening

300
Q

What are the 2 types of esophageal cancer

A

Adenocarcinoma

Squamous cell carcinoma

301
Q

What is adenocarcinoma complications of

A

GERD and Barrett esophagus

302
Q

Where does adeocarcinoma occur

A

Distal 1/3 esophagus

(White males)

303
Q

Where does squamous cell carcinoma occur

A

Middle part of esophagus (top 2/3)

304
Q

What are the risk factors for squamous cell carcinoma

A 
Alcohol
Tobacco
Injury
Achalasia
Consumption of hot beverages
305
Q

What are the common presentations of esophageal cancer

A 
Dysphagia**
Weight loss
Anorexia
Fatigue
Pain on swallowing
306
Q

How do you treat esophageal cancer

A

Depends on the stage

Early: surgical resection/radiation/chemo

Long term survival is limited

307
Q

What is food churned with in the stomach

A

HCl and pepsin

308
Q

What is the gastric mucosal barrier

A
  • Lining that is impermeable to acid it secretes

- there is coupled secretion of H+ ad HCO3- ions

309
Q

Gastric mucus is _____

A

Protective

310
Q

Why are cells closely packed in gastric muscular barrier?

A

To prevent acid penetration and covered with an impermeable hydrophobic layer

There is no diffusion of ionized water soluble molecules

311
Q

What disrupts the gastric barrier

A

Aspirin and bile

312
Q

What protects the stomach wall

A

Prostaglandins

313
Q

What is gastritis

A

Inflammation of gastric mucosa

314
Q

What are the causes of gastritis

A 
Aspirin, alcohol, NSAIDs
Bacterial toxins
Oral corticosteroids
Serious illness/trauma with stress
Radiotherapy
Chemo
315
Q

What are some causes of acute gastritis

A

Spirit
Alcohol
Toxins (s. Aureus)

316
Q

What causes black/tarry stools in acute gastritis

A

Hemorrhage

317
Q

What is chronic gastritis

A

Presence of chronic inflammation leading to atrophy

Absence of grossly visible erosions

318
Q

What are the 3 types of chronic gastritis

A
  1. Helicobacter pylori gastritis
  2. Autoimmune gastritis
  3. Chemical gastropathy
319
Q

What resolves acute gastritis

A

Removal of the cause of it

320
Q

What is the most common cause of gastritis in the US

A

Helicobacter pylori gastritis

321
Q

How does H. Pylori cause gastritis

A

It produces enzymes and toxins leading to inflammation, atrophy, and metaplasia

322
Q

Gram stain of H. Pylori

A

Red

323
Q

How do you treat H. Pylori gastritis

A

2-3 Ab with a Proton pump inhibitor

324
Q

What causes autoimmune gastritis

A

Rare (10%)

Autoantibodies to gastric cells and intrinsic factor

Causes anemia, atrophy, and adenocarcinoma

Chronic injury is due to alkaline duodenal reflux

325
Q

What is peptic ulcer disease

A

Involve gastric muscle and proximal duodenum

Can affect one or all 3 layers of the stomach

Regeneration is imperfect with scarring

326
Q

What are the risk factors for peptic ulcer disease

A 
H. Pylori
NSAIDs
Corticosteroids
Smoking
Genetics
327
Q

What are the symptoms o peptic ulcer disease

A

Epigastric discomfort and pain

Periodic pain is the hallmark

328
Q

What are teh complications of peptic ulcer disease

A

Hemorrhage
Perforation
Gastric outlet obstruction

329
Q

How do you treat PUD

A

Eradicate cause

330
Q

What is Zollinger-Ellison Syndrome

A

Rare condition with irresectable gastronomes in duodenum and pancreas

2/3 are malignant
1/3 have metastasized by time f diagnosis

331
Q

What are curling ulcers

A

Caused by major physiological stress like burns, trauma, sepsis, severe liver failure, major surgical procedures

332
Q

What are Cushing ulcers

A

Gastric, duodenum, and esophageal ulcers in persons with intracranial injury
Increased ICP causes vagal stimulation and hypersecretion of acid

333
Q

What is the 15th leading cause of death

A

Stomach cancer

334
Q

What are the risk factors fro stomach cancer

A

Genetics
Carcinogens
Autoimmune gastritis
Gastric adenoids/polyps

335
Q

What are the symptoms of stomach cancer

A

Vague

DETECTION is difficult

336
Q

What is the diagnosis for stomach cancer

A

Ba X ray
Endoscopy/biopsy
Cytologic studies

337
Q

What it’s eh treatment for stomach cancer

A

Radical gastrectomy
Irradiation
Chemo

338
Q

What is the #1 autoimmune disorder in the US

A

Celiac disease

339
Q

What triggers celiac disease

A

Ingestion of gluten containing grains

340
Q

What kind of immune repsonse is is celiac disease

A

T cell mediated

There is an increased level of Ab

341
Q

What are the symptoms/signs of celiac disease

A

Diarrhea
Pruritic rash
Itching/burning
Abdominal pan

Bloating
Irritability/depression
Stomach upset
Joint pain
Muscle cramps
Skin rash
Mouth sores
Dental/bone disorders
Tingling of legs/feet
342
Q

How do you diagnose celiac disease

A

case Hx
IgA- antitTG test

Biopsy

Flattened brow

343
Q

What is lactose intolerance

A

You dont have lactase enzyme to break down lactose, so it gets fermented by gut bacteria and causes gas, and abdominal pain

344
Q

How is lactose intolerance managed

A

Limit dairy product intake

Use a substitute nutrient source to maintain energy and protein intake

Use lactose products

Eat yogurt with live and active cultures

345
Q

What are the 2 related chronic inflammatory disorders

A

Chrohn’s

Ulcerative colitis

346
Q

Where is Crohn’s disease localized

A

Any part of GI tract except the rectum

SKIP lesions

347
Q

Where does ulcerative colitis localize

A

Colon
Continuous inflammation
Rectum is involved

348
Q

Where is the pain in Crohn’s disease

A

Lower right abdomen

349
Q

Where is pain in ulcerative colitis

A

Lower left abdomen

350
Q

What is the morphology of Crohn’s disease

A 
Colon wall is thickened
Transmural inflammation
Cobblestone mucosa
Ulcers
Fistula
351
Q

What is the morphology of ulcerative colitis

A 
Colon wall is thinner
Mucosal inflammation
Pseudopolyps
Crypt abscesses
Ulcers
352
Q

What are the complications of Crohn’s disease

A 
Strictures
Fistulas
Perianal disease
Malabsorption 
Nutritional depletion
353
Q

What are the complications of ulcerative colitis

A

Severe stenosis
Toxic megacolon
Colorectal carcinoma

354
Q

Is bleeding common in Crohns

A

No

355
Q

Is bleeding common in ulcerative colitis

A

Yes

356
Q

What are the ocular findings with Crohns

A

Non-granulomatous uveitis

1-10%

357
Q

What are the ocular findings in ulcerative colitis

A

Non-granulomatous uveitis

1-5%

358
Q

How do you treat Crohns and ulcerative colitis

A

Anti-inflammatorys
Immunosuppressive agents
Steroids
Surgery

359
Q

What is the prognosis for Crohns and ulcerative colitis

A

Chronic

Constant monitoring

360
Q

What is IBS

A

Recurrent abdominal pain or discomfort 3 days/month for the past 3 months with symptoms onset of more than 6 month.

361
Q

What is associated with IBS

A

Pain relief with defecation
Change in bowel habits
Change in stool form

362
Q

Who is most affected by IBS

A

Females

363
Q

What can trigger IBS

A

Stress

364
Q

What foods can trigger IBS

A

Processed food
High fructose corn syrup
Milk formulas in infants

365
Q

How do you treat IBS

A

Stress management
Increase fiber
Avoid fatty, gas producing foods, alcohol, and caffeine

Antispasmotics
Anticholinergics
Serotonin antagonist

366
Q

Heterochromia

A

Wtf??

2 different colored eyes….

367
Q

What is diverticulitis

A

Acquired her nations of the colonic mucosa and submucosa through the muscularis propria

Occurs most commonly in the sigmoid colon

368
Q

What is diverticulosis

A

Presence of diverticula in an individual who is asymptomatic

369
Q

What is diverticular disease

A

Reserve of diverticula associated with symptoms

20% of individuals with diverticula

370
Q

What are the symptoms of diverticulosis

A

Abdominal pain (LL quad)
N/V
Tenderness
Fever

371
Q

How do you diagnose diverticulosis

A 
Case Hx
Barium enema
CT scan
Endoscopy
Ultrasound
372
Q

What are the complications of diverticulosis

A 
Diverticulitis
Perforation with peritonitis
Abscess
Hemorrhage
Bowel obstruction
Fistulas
373
Q

What is appendicitis

A

Inflammation of the appendix

374
Q

What are the symptoms of appendicitis

A

Periumbilical pain (dull and steady)

Low grade fever
Nausea
Anorexia

375
Q

What does sudden pain relief in appenditcitis indicate

A

Rupture of appendix

But they can have rebound pain or tenderness

376
Q

What is the #1 cancer of GIT

A

Colorectal adenocarcinoma

377
Q

What are the risk factors for colorectal cancer

A 
Age
Family Hx of cancer
Crohn’s disease or ulcerative colitis
Familial adenomatous polyposis
Diet
378
Q

What can help protect you from colorectal cancer

A

Vitamin A, C, E

379
Q

What is the presentation of colorectal cancer

A

Symptoms come later
Bleeding**

Change in bowel habits
Diarrhea
Constipation
Sense of urgency
Sense of incomplete emptying
PAIN is later
380
Q

How do you treat colorectal cancer

A

Surgical removal

Radio/chemotherapy

381
Q

What is the prognosis for colorectal cancer Stage 1

A

5 year survival rate of 90-100%

382
Q

What is the prognosis for stage 4 colorectal cancer

A

Metastatic

Poor prognosis

383
Q

Prevention is key!!

A

We are what we eat

Eat a fresh healthy diet
Avoid irritants

384
Q

For stage 3 colorectal cancer how do you treat it

A

Do radiation to reduce the size

Then surgery

385
Q

How do you treat stage 4 colorectal cancer

A

Surgery

Then radiation therapy

Pathology (4 decks)

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