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Patho > Patho Exam 1 > Flashcards

Patho Exam 1 Flashcards

1
Q

What are varicose veins?

A

They are veins in which the blood has pooled

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2
Q

What causes varicose veins to develop?

A

Trauma or gradual venous distension render the valves incompetent and decrease their capacity to push blood back toward the heart

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3
Q

What’s the difference between primary varicose veins and secondary varicose veins?

A

Primary varicose veins originate in superficial saphenous muscle while secondary varicose veins result from impaired blood flow in deep venous channels, such as DVTs

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4
Q

What is mycoardial ischemia?

A

When the coronary blood supply can’t meet the oxygen and nutrient demands of the myocardium

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5
Q

What are nonmodifiable risk factors for developing CAD? (2)

A
  1. age

2. fam history

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6
Q

What are modifiable risk factors for developing CAD? (7)

A
  1. dyslipidemia
  2. HTN
  3. smoking
  4. DM/insulin resistance
  5. obesity
  6. sedentary lifestyle
  7. atherogenic diet
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7
Q

What are nontraditional risk factors for developing CAD? (4)

A
  1. CRP - a serum marker for inflammation
  2. serum homocysteine - derived from the metab of an amino acid that is abundent in animal protein
  3. serum lipoprotein - similar in composition to LDL
  4. infectious agents
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8
Q

How does Nicotine increase risk for atherosclerosis? (4)

A

1) causes vasoconstriction
2) causes endothelial damage
3) causes an increase in LDL
4) causes a decrease in HDL

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9
Q

What comprise LDLs?

What role does LDL play?

A

LDLs are comprised of cholesterol and a carrier protein

LDLs deliver cholesterol to tissues

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10
Q

What comprise HDLs?

What role does HDL play?

A

HDLs are comprised of a phosholipid and a carrier protein

HDLs are responsible for reverse cholesterol transport – return excess cholesterol from tissues to the liver where it is eliminated as bile or converted into steroids.

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11
Q

What’s the relationship between HDLs and atherosclerosis

A

HDLs helps combat atherosclerosis by removing cholesterol from arterial walls

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12
Q

What is prinzmetal angina?

How does it present?

Why is it dangerous?

A

Prinzmetal angina is a kind of angina that causes unpredictable chest pain

It usually occurs at rest or with minimal exercise. It often occurs nocturnally.

It’s dangerous because it’s known cause serious arrythmias and ECG changes during episodes

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13
Q

What is the difference between MI and unstable angina?

A

During an MI, ischemia is severe enough to cause myocardial damage and tissue necrosis that results in the release of detectable levels of troponin and CKMB. In unstable angina, ischemia is transient enough that reperfusio occurs before tissue necrosis takes place. You therefore won’t see serum troponin and CKMB.

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14
Q

Describe the pathophysiology of what happens after an MI:

  • -4 hours after?
  • -12-24 hours after?
  • -1-3 days after?
  • -4-7 days after?
  • -7-10 days after?
A

4 hours after infarct: myocytes without adequate blood supply arent able get rid of toxic waste. They become very leaky/self destruct. this causes release of enzymes like troponin
12-24 hours: neutrophils enter infarcted area and start clean up
1-3 days: LOTS of neuts lysing all the old myocytes
4-7 days: neuts die and macrophages come in to remove necrotic tissue and cellular debris. This is when the myocardial wall is weakest and at highest risk for rupture
7-10 days: small blood vessels start to grow into infarcted area, allowing for fibroblasts to lay down structural collagen proteins. We call this granulation tissue
1-1.5 months: collagen tissue is replaced by Type 1 collagen, which is noncontractile scar tissue

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15
Q

What is cardiac remodeling?

A

After an MI the myocardial wall changes in size, shape and thickness. Nonfunctioning muscle in infarcted area becomes thinner and dilated. The muscle around it becomes thicker as it compensates for the infarcted area.

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16
Q

What serum biomarkers do we see elevated after an MI? (3)

How long after an MI do we see each?

For how long does each remain elevated?

A

Troponin 1, Troponin T, and CKMB

Trop 1 and Trop 2 rise within 3 hours of onset and remain elevated for 7-10 days.

CKMB rise within 4-8 hours and decline to normal within 2-3 days

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17
Q

Which cardiac biomarker is more reliable in indicating an MI?

A

Troponins

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18
Q

What EKG changes are associated with myocardial ischemia? (3)

A
  1. ST segment depression
  2. T wave inversion
  3. ST segment elevation
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19
Q

What role does angiotensin II play systemically after a MI?

A

An MI triggers the SNS, which triggers the RAAS. The RAAS activates angiotensin II, which causes peripheral vasoconstriction and fluid retention. This increased peripheral vascular resistance and increased blood volume increases the workload of the heart and exacerbates the loss of myocardial contractility

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20
Q

What are the effects of angiotensin II locally on the myocardium during and immediately after a MI?

  • -1 good thing
  • -1 good and bad thing
  • -1 bad thing
A

Good thing: it’s a growth factor for smooth muscle cells, myocytes, and fibroblasts
good and bad thing: promotes release of catecholamines (epi and norepi)
bad thing: causes coronary artery spasms

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21
Q

How is Ang II contribute to cardiac remodeling

–2 things

A
  1. it’s a growth factor for myocites, so contributes to hypertrophy of myocardium around infarcted area
  2. growth factor for fibroblasts, so contributes to development of noncontractile scar tissue
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22
Q

What is right sided HF

Manifestations of R sided heart failure:

  • what’s the hallmark sign?
  • blood might also back up into what important organ system?
A

Right sided HF is an inability of the heart to move deoxygenated blood coming in from systemic circulation into pulmonary circulation

RHF manifests as an accumulation of blood in systemic circulation,

  • hallmark sign: peripheral edema
  • may also see backup of blood into the hepatic veins, causing hepatomegaly and potentially RUQ pain.
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23
Q

What are 2 causes of R sided HF?

A
  1. left ventricular dysfunction

2. pulmonary HTN

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24
Q

What is cor pulmonale?

A

When R HF occurs in response to chronic pulmonary disease.

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25
Q

What is preload?

A

Preload is the volume of blood entering the heart and stretching the ventricles when theyre full at the end of diastole

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26
Q

What can increase preload? (2)

A

1) decreased contractility or 2) increased blood volume

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27
Q

What is systolic dysfunction?

A

Systolic dysfunction represents a decrease in myocardial contractility and an impaired ability to eject blood from the L vent

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28
Q

Define systolic HF in terms of EF

A

When you have an EF of less than 40%

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29
Q

Describe how the SNS responds to a decrease in CO associated with systolic HF

  • -which hormones are involved? (2)
  • -what are the effects? (4)
A

A decrease in CO triggers SNS response.

The SNS releases catecholamines like
1) epi and 2) norepi

Epi and norepi:

1) increase HR
2) increase contractility
3) increase vascular tone
4) trigger RAAS, which enhances renal Na and water retention

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30
Q

Describe how systolic HF triggers the RAAS (2 ways)

What effects does Ang II have during acute of systolic HF (2)

A
  1. epi and norepi trigger the RAS
  2. decreased blood flow to the kidneys triggers the release of renin from the kidneys, which starts the chain reaction and production of Ang II

Effects of Ang II:

1) Ang II causes retention of Na and H20, increasing blood volume and thus increasing preload
2) Ang II inhibits reuptake of norepi by SNS, further increasing its presence in circulation

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31
Q

Describe why you see higher levels of circulating aldosterone in patients with systolic HF

A

Aldosterone is typically broken down by the liver. If you have liver congestion from 2/2 systolic HF, then it may not be broken down properly.

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32
Q

What are ANP and BNP and when are they released?

A

ANP is a peptide released by the atria in response to stretch, so often in response to increased preload/fluid overload

BNP is a peptide released by the vents in response to increased pressure or fluid overload.

So you see higher levels of ANP and BNP in patients w heart failure as the chambers become distended with too much volume.

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33
Q

What are the systemic effects of BNP specifically?

What are the systemic effects of ANP and BNP?

A

BNP promotes rapid dieuresis by increasing glomerular filtration - helps to combat fluid overload

Both ANP and BNP inhibit the SNS and RAAS – so assist in reducing the workload on the heart and decreasing blood volume

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34
Q

What is angina pectoris?

A

Precordial or substernal chest pain that is caused when blood/oxygen supply to coronary arteries doesn’t meet the oxygen demands of the myocardium.

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35
Q

What commonly triggers angina pectoris? (3)

A
  1. Physical exertion
  2. cold
  3. emotional stress
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36
Q

What is acyanotic CHF?

A

An inability of the heart to supply body with blood borne nutrients despite adequate blood volume and normal or elevated myocardial contractility

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37
Q

What are common causes of acyanotic CHF? (4)

A
  1. anemia
  2. septicemia
  3. hyperthyroidism
  4. beri beri
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38
Q

What congenital chromosomal disorders are associated with acyanotic CHF? (3)

A
  1. trisomy 13
  2. trisomy 18
  3. trisomy 21 (down’s syndrome)
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39
Q

Tell me about the pathophysioogy of VSD

A

Ventricular septal defect is a congenital defect in which there is an opening between the R and L ventricles. Oxygenated blood in the high pressure left ventricle gets shunted into the low pressure R ventricle.

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40
Q

Is VSD usually symptomatic?

A

Nah.

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41
Q

Under what circumstances is VSD symptomatic?

How does this develop?

How does sympatomatic VSD present? (3)

A

VSD may become symptomatic in a very large L –> R shunt.

Typically develops a few weeks after birth when pulmonary vascular resistance starts to fall.

Presentation: tachypnea, diaphoresis (esp when eating), failure to thrive

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42
Q

What two factors can cause or contribute to HTN?

A
  1. increased cardiac output

2. increased systemic vascular resistance

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43
Q

Tell me about the pathophysiology of primary HTN

  • -which hormonal systems are involved? (2)
  • -what are the physiologic effects?
A
  • overactive SNS
  • overactive RAAS

Physiologic effects:
SNS: increased HR and increased contractility, so increased CO
RAAS: vasoconstriction, salt/fluid retention,

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44
Q

The presence of Virchow’s Triad increases the risk for what CV disorder?

A

DVTs!

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45
Q

What 3 things comprise Virchow’s Triad?

A

1 ) stasis of venous flow due to inactivity of skeletal muscle pumps

2) hypercoaguable state resulting from a decrease in vascular volume , increase in blood viscosity, and increase in blood coagulation factors
3) vessel injury to the endothelium resulting from external pressure from the veins

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46
Q

What is aortic stenosis?

A

When the aortic valve becomes stiff or narrowed, therefore increasing the amount of pressure the left ventricle must generate to push blood through it and into systemic circulation.

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47
Q

At what point does aortic stenosis become symptomatic?

A

When the valve area is reduced to 1/4 of it’s normal size

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48
Q

Once symptomatic, how does aortic stenosis present? (5)

A
  1. loud systolic ejection murmur
  2. split second heart sound as the aortic valve closes more slowly than the pulmonic valve
  3. angina
  4. syncope
  5. exertional dyspnea
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49
Q

What are the 3 causes of pulmonary emboli?

A

1) venous stasis
2) vessel injury
3) hypercoagulability

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50
Q

How do venous stasis, vessel injury, and hypercoagualbility contribute to the development of a PE?

A

They all increase the risk for the development of a thrombus, which can become dislodged and travel into pulmonary circulation, totally or partially occluding a pulmonary vessel

51
Q

What are the 3 primary characteristics of asthma?

A
  1. bronchoconstriction
  2. mucosal edema
  3. increased mucous production
52
Q

Tell me the pathophysiology of the early asthmatic response

–keep in mind what kinds of cells are involved and who triggers who and who releases what

A
  1. B cells differentiate into plasma cells
  2. Plasma cells produce IgE
  3. IgE responds to the presence of the allergen, presenting the allergen’s antibody to a mast cell
  4. mast cells release histamine and inflammatory mediators
53
Q

Let’s talk about the interleukins implicated in the early asthmatic response

First, which interleukins are implicated?

A 
IL 5
IL 8
IL 13
IL 17
IL 22
54
Q

What does IL 5 do? (2 things)

What does IL 8 do? (1 thing)

What does IL 13 do? (3 things)

What does IL 17 do? (1 thing)

What does IL 22 do? (1 thing)

A

IL 5: 1) activates eosinophils, which contribute to bronchial 2) hyper responsiveness

IL 8: activates neutrophils

IL 13: 1) impairs mucociliary clearance, 2) enhances fibroblast secretion, 3) contributes to bronchoconstriction

IL 17: perpetuates neutrophillic inflammation

IL 22: simulates epithelial cells

55
Q

What interleukins are implicated in early asthmatic response and what are their effects? (4)

A

1) IL 8 – activates neurtrophils
2) IL 13 –
3) IL 17 – increases neutrophilic inflammation
4) IL 22- stimulates epithelial cells, promoting immune response

56
Q

When does what we call the late asthmatic response begin and end?

A

4-8 hours after exacerbation begins

57
Q

What characterizes the late asthmatic response? (4)

A
  1. prolonged smooth muscle contraction
  2. hyperresponsive airway
  3. mucous plugging which leads to air trapping and hyperinflation
  4. hypoxemia
58
Q

What happens to the airway if asthma is left untreated?

A

Airway scarring and remodeling

59
Q

How does an asthma exacerbation present? (6)

A
  1. expiratory wheezes
  2. nonproductive cough
  3. prolonged expiration
  4. dyspnea
  5. tachypnea
  6. tachycardia
60
Q

Tell me about mucous production as it relates to chronic bronchitis

A

Inspired irritants (like smoke) increase mucous production as well as the size and number of mucous glands. The mucous produced is thicker than normal.

61
Q

What happens to bronchial smooth muscle as chronic bronchitis develops?

A

It hypertrrophies

62
Q

What happens to the elasticity of the lung fibers and alveolar tissues as chronic bronchitis progresses? How does this manifest?

What happens to alveolar tissues as a result? Why is this so important?

A

lung fibers and alveolar tissues become less elastic, which leads to airway collapse during expiration and the trapping of air in the lungs

Alveolar tissues become damaged, which decreases the surface area available for gas exchange

63
Q

What are the two prominent characteristics of chronic bronchitis on presentation?

A
  1. increased mucous

2. chronic cough

64
Q

How long must a productive cough last in order for it to be considered chronic bronchitis?

A

For at least 3 months of the year for at least 2 consecutive years

65
Q

How may a patient with chronic bronchitis present? (5)

A
  1. decreased exercise tolerance
  2. wheezing and shortness of breath
  3. productive cough
  4. polycythemia
  5. decreased FEV1 (because of air trapping)
66
Q

Define emphysema

A

the abnormal permanent enlargement of gas-exchange airways and destruction of alveolar walls

67
Q

Outline for me the patho of emphysema

  • -we see a break down of what?
  • -and what causes this breakdown? (3)
  • -this breakdown leads to the destruction of what?
  • -and this destruction produces what?
A
  • we see a breakdown in elastin caused by 1) imbalance between proteases and antiproteases 2) oxidative stress, and 3) apoptosis of the lung’s structural cells causes a break down in elastin
  • this breakdown of elastin leads to destruction of alveoli.
  • Alveolar destruction produces large air spaces within the lung parenchyma called bullae and air spaces adjacent to the pleurae called blebs.
68
Q

What are the clinical manifestations of emphysema?

A
  1. DOE, progressing to dyspnea at rest
  2. tachypnea with prolonged expiration – see pursed lip expiration
  3. use of accessory muscle s
  4. barrel chest
  5. tripod position
69
Q

What do we NOT see with emphysema that we do see in chronic bronchitis? (2 things)

A

cough or excessive mucous

70
Q

What commonly precedes the development of pneumonia?

How does pneumonia typically present? (6)

A

URI

  1. cough
  2. dyspnea
  3. fever
  4. chills
  5. malaise
  6. pleuritic chest pain
71
Q

What is croup exactly in just two words

A

Acute laryngotracheobronchitis

72
Q

In what patient population do we typically see croup?

A

kids aged 6 months to 3 years

73
Q

What pathogen most commonly causes croup?

What other pathogens also cause it? (2)

A

Most commonly caused by viral Parainfluenza. Can also be caused by influenza A or RSV.

74
Q

What’s the most significant and dangerous clinical manifestation of croup?

A

Croup can cause inflammation/edema of the subglottic area, which can lead to respiratory obstruction

75
Q

What are the hallmark symptoms of croup? (2)

A

Seal like cough, inspiratory stridor

76
Q

What virus typically causes epiglotitis?

A

haemophilus influenza type B (HIB)

77
Q

What’s happening pathophysiologically with epiglotitis?

A

characterized by inflammation of the epiglottis and pharyngeal structures

78
Q

Does epiglotitis have a sudden or gradual onset?

A

Sudden

79
Q

how does child with epiglotitis commonly sit?

A

sits up with mouth open and chin thrust forward

80
Q

how else does child with epiglotitis commonly appear? (7)

A
  1. pale,
  2. lethargic
  3. dysphagia/difficulty swallowing
  4. muffled voice
  5. drooling
  6. fever
  7. anxious
81
Q

How do you dignose epiglotitis?

–whats the big thing to know here?

A

You diagnose it based on physical exam. But you do NOT want to examine the throat until you have airway management nearby because this could trigger laryngospasm and total obstruction/respiratory arrest.

82
Q

Tell me about the patho of GERD

A

You have decreased resting tone of the lower esophageal sphincter, which leads to reflux of acid and pepsin from the stomach into the esophagus, causing esophagitis.

83
Q

How do we diagnose GERD?

A

based upon clinical presentation

84
Q

And how does GERD present? (4)

A
  1. heartburn/epigastric pain
  2. cough
  3. hoarseness
  4. upper abdominal pain within 1 hour of eating
85
Q

What is our first line of treatment for GERD?

A

lifestyle modifications

86
Q

What are 3 complications of GERD?

A
  1. barrett’s esophagitis
  2. esophageal cancer
  3. peptic stricture
87
Q

What is gastritis?

A

Inflammation of the gastric mucosa

88
Q

What can cause gastritis? (7)

A
  1. H Pylori
  2. NSAIDS
  3. alcohol
  4. bile reflux
  5. bacteria
  6. autoimmune response
  7. mucosal ischemia
89
Q

How can chronic gastritis present? (5)

A
  1. anorexia
  2. fullness
  3. nausea/ vomiting,
  4. epigastric pain
  5. gastric bleeding
90
Q

Tell me about the pathophysiology of chronic fundal gastritis

A

chronic fundal gastritis is also known as autoimmune gastritis. Autoantibodies are presented to components of gastric gland parietal cells and intrinsic factor. The gastric gland and mucosal atrophy lead to a loss of acid production.

91
Q

What happens to the production of B12 in severe cases of chronic fundal gastritis?
–what effect does this have?

A

In severe cases you’ll also see a loss of production of intrinsic factor, which leads to a deficiency in B12 and pernicious anemia

92
Q

Chronic fundal gastritis is often associated with which autoimmune disorders? (3)

A
  1. hashimoto
  2. Addison disease
  3. Graves disease
93
Q

Chronic gastritis can affect which parts of the stomach?

What typically causes chronic fundal gastritis?

What typically causes chronic antral gastritis?

Chronic antral gastritis increases the risk for which other gastric DO?

A

The fundus or the antrum

Chronic fundal gastritis usually caused by autoimmune disorder

Chronic antral gastritis is usually caused by H pylori or NSAIDs

Chronic antral gastritis increases risk for PUD

94
Q

what are peptic ulcers?

A

The breakdown or ulceration in the protective mucosal lining of the lower stomach, esophogus or duodenum

95
Q

What typically causes duoendal peptic ulcers

A

H Pylori

96
Q

What typically causes gastric peptic ulcers?

A

NSAIDS

97
Q

Are peptic ulcers typically caused by increased acid production or decreased mucous protect?

A

decreased mucous protection!

98
Q

If ulcers are duodenal, when do you typically experience pain?

A

30 min to 2 hours after eating, when stomach is empty. Food relieves pain.

99
Q

If ulcers are gastric, when do you typically experience pain?

A

immediately after eating. So patients often eat less, causing weight loss.

100
Q

What are 7 risk factors for developing PUD?

A
  1. alcohol
  2. smoking
  3. acute pancreatitis
  4. COPD
  5. obesity
  6. cirrhosis
  7. age (over 65)
101
Q

What is a sliding hiatal hernia?

A

A bell shaped protrusion of the upper part of the stomach through the diaphragm and into the thorax

102
Q

How does a patient with sliding hiatal hernia often present?

A

Often asymptomatic, but may present with heartburn, regurg, epigastric pain, dysphagia

103
Q

What may cause a sliding hiatal hernia?

A
  • injury, trauma, surgery

- persistent pressure on the surrounding muscles such as when coughing, vomiting, pooping, or lifting heavy objects

104
Q

What is paraesophogeal hiatal hernia?

A

When a separate portion of the stomach, usually along the greater portion of the stomach, enters the thorax through a widened opening and then progressively enlarges. This can cause more serious complications and may need surgical repair.

105
Q

What is a cushing ulcer?

What can cause it?

A

A kind gastric, duodenal or eosphogeal stress ulcer that arises in a person with intracranial injury, surgery, or tumors.

Cushing ulcers result from hypersecretion of gastric acid resulting from stimulation of the vagal nuclei by increased intracranial pressure.

106
Q

What is portal HTN?

A

abnormally high blood pressure in the portal venous system. Pressure is at least 10, compared to normal of 3 mmHg

107
Q

How does portal HTN manifest clinically? (3)

A

obstruction of blood flow in the portal vein results in

1) increased hydrostatic pressure in peritoneal capillaries, causing ascites,
2) splenic engorgement with sequestration and destruction of RBCs and platelets,
3) shunting of blood into collateral venous channels.

108
Q

Tell me about varices in relation to portal HTN.

–what are they?

A

When blood cant enter the portal vein due to higher pressure, the body develops collateral circulation into the liver to deliver blood back to the SVC. But these vessels have thin walls that can’t withstand high pressure. They become

109
Q

Tell me about varices in relation to portal HTN.

–where do we usually find them?

A

Lower esophagus, stomach, rectum

110
Q

Tell me about varices in relation to portal HTN.

–why are they so dangerous?

A

Because they can be life threatening of they rupture

111
Q

How much a patient with a ruptured esophogeal varice present?

A

Vomiting blood

112
Q

Tell me about the patho behind cirrhosis of the liver.

A

Cirrhosis is the end stage of chronic liver disease. It’s characterized by diffuse fibroids and conversion of normal liver into nodules containing proliferating hepatocytes encircled by fibrosis. This fibrous tissue forms constrictive bands that obstruct flow through vascular channels and the biliary tree. The disruption of of vascular channels causes portal HTN.

113
Q

What is pyelonephritis?

A

acute infection of the ureter, renal pelvic, and/or renal parenchyma

114
Q

How does pyelonephritis present? (5)

A
  1. flank pain
  2. fever
  3. chills
  4. costovertebral tenderness
  5. purulent urine
115
Q

What does chronic pyelonephritis lead to?

A

leads to scarring and fibrosis of the kidneys and chronic kidney failure

116
Q

What diagnostic tests may we want to do if we suspect pyelonephritis?

A

UA looking for WBC casts

117
Q

What’s the cause of anemia as it relates to renal failure?

A

Kidneys are primary site for production of erythropoietin, so when in renal failure not enough erythropoietin is produced to stimulate the bone marrow to produce adequate RBCs. We also may see blood loss during dialysis

118
Q

What are kussmaul respirations?

Under what circumstances do we see this respiratory pattern and why?

A

Kussmaul respirations are deep rapid respirations, patients breathes as though they’ve been running

See this pattern mostly in patients with DKA/metabolic acidosis – the respiratory system compensates for a decrease in pH by increasing ventilation to reduce PCO2.

119
Q

What;s the patho behind Down Syndrome?

A

caused by nondisjunction or an error in cell division during meiosis, causing a trisomy of chromosome 21

120
Q

How does Down Syndrome present/manifest? (11)

A
  1. epicanthal folds/slanted eyes
  2. flat facial profile/flat occiput
  3. malformed ears
  4. big protruding wrinkled tongue
  5. short broad hands
  6. wide gap between first and second toes, 7. congenital heart disease,
  7. acute lymphoblastic leukemia
  8. intestinal malformations
  9. growth failure
  10. mental retardation
121
Q

What is the patho of Turner Syndrome?

A

absence of all or part of the X chromosome

122
Q

How does Turner Syndrome present/manifest? (8)

A

1) short in stature but with nomal proportions
2) webbed neck
3) problems with hearing/vision
4. small mandible
5) lose the majority of their oocytes by age , so do not menstruate and show no signs of secondary sec characteristics
6) cardiac abnormalities including bicuspid aortic valve or coarctation of the aorta
7) horseshoe kidney
8) shield chest with widely spaced nipples

123
Q

Tell me about autosomal recessive trait inheritance

A

These traits manifest only when both members of the gene pair are affected – so both parents may be unaffected but are carriers of the defective gene and can pass it on to their children

124
Q

What are two common autosomal recessive disorders?

A

Phenylketonuria - caused by a deficiency in a liver enzyme that results in build up of amnio acids, phenylalaline to accumulate in blood and tissues . if untreated, results in mental retardation, microcephaly, delayed speech, and other neurologic dysfunction. Infants are regularly screened.

Tay Sachs – kids appear normal at birth and begin to manifest progressive weakness, muscle flaccidity and decreased attentiveness at 6-10 months. Death usually occurs at 4-5 yaers of age

Patho (2 decks)

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