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Low Yield Semmelweis > Lectures Pathophys Questions > Flashcards

Lectures Pathophys Questions Flashcards

1
Q

What are the consequences of Chronic Right Heart failure

A

Systemic Congestion - Hepatomegaly, Splenomegaly, Renomegaly
Skin cyanosis
Acites

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2
Q

What are the consequences of Chronic Left Heart failure

A

Congestion of the Lungs
Heart Failure cells in sputum
Dyspnea

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3
Q

Definition of Shock

A

State of significant Hypo-perfusion resulting in a cell Injury due to Hypoxia and lack of waste metabolites removal

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4
Q

Short term effects of Shock

A

Syncope, Orthostatic collapse, Carotis Hyperesthesia, Electric shock, Spinal cord Injury

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5
Q

Stages of shock

A

Compensated - maintaining perfusion.
Progressive - Inadequate perfusion levels start to show.
Irreversible - Cell and tissue damage, Multi-organ failure.

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6
Q

Pathophysiology of Shock - Progression of events in the various stages

A

Stage 1 - Pathogenesis causes low CO or low TPR, Hypotension compensated.
Stage 2 - Decreased perfusion and Major end-organ dysfunction, Hypotension Decompensated.
Stage 3 - Microcirculatory failure and endothelial damage leading to cellular membrane Injury and death.

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7
Q

Clinical markers of shock

A 
Brachial systolic BP - less than 100mmHg
Sinus Tachycardia
Metabolic Acidemia
Hypoxemia
Low urine output and High respiratory rate.
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8
Q

Classification of shocks

A

Hypovolemic shock - Loss of blood or body fluids
Obstructive shock - Embolism
Cardiogenic Shock - Heart failure
Distributive Shock - Neurogenic, Anaphylactic, Septic

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9
Q

Shock Index

A

SI = RR Interval divided by Pulse
Should be 2 a Normal conditions.
It is lower than 1 in case of shock.

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10
Q

Further classification of Irreversible and Progressive stages of shock

A

Subacute reversible - Oxygen delivery could overtime return to normal with medical attention
Subacute Irreversible - with time and medical care no normal oxygen delivery could be achieved, although an initial improvement may appear.
Acute Irreversible - No Improvement whatsoever and only deterioration of the supply and demand of oxygen ratio.

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11
Q

Hypovolemic shock - causes

A

Hemorrhage, Vomiting or Diarrhea, Diabetes or Diuretics, Burns or Inflammation of skin, Loss of interstitial fluids

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12
Q

Hemorrhagic shock Initial Compensation - Neural

A

Alpha Adrenergic- Vasoconstriction of GI, Muscle, Adipose, KIdney vessels
Beta Adrenergic- Bronchodilation and cardiac stimulation
Pale skin, Decreased Diuresis, Muscle weakness

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13
Q

Hemorrhagic shock - Progressive Compensation efforts, Humeral

A

Blood Glucose elevation and Capillary pressure lowering.

ADH and Renin-Angiotensin- Aldosterone sys

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14
Q

Hemorrhagic Shock - Irreversible stage

A

Cell death metabolites diffuses easily to systemic circulation due to high vasodilation causing irreversible damage and death

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15
Q

Cardiogenic shock cause and possible treatment

A

Heart (pump) Failure - 40% of Myocardium damaged by AMI

Alternative Pumping - Transplant or Synthetic Device

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16
Q

Distributive Shock - symptoms

A 
Normovolmia
Normotension 
Low TPR
High CO
Redness fever
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17
Q

Distributive Shock
Septic
Causes and Events

A

The same events of Anaphylactic shock occur due to overwhelming infection reactions.

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18
Q

Distributive Shock
Anaphylactic
Causes and Events

A

Immunogenic Inappropriate Vasodilation causes fluid shift into cells from capillaries.
Micro clots are formed and hazardous SMC contraction occurs like Bronchospasm.

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19
Q

Distributive Shock
Neurogenic
Causes and Events

A

Spinal cord Lesion, Poisoning or Drug abuse causing inability of NS to maintain Vascular tone.

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20
Q

Hyperdynamic stage of Distributive Shock

A

Accumulation of Lactic Acid
Changes in Amino acid metabolism - Tyrosine becomes Octopamine that inhibits alpha receptors
Increased NO - By cytokines
Relative oxygen deficits - Cardiac failure

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21
Q

Obstructive Shock causes

A

Pulmonary Embolism - Blocked pulmonary Circulation
Tension Pneumothorax - Increased Intrathoracic Pressure
Cardiac Temponade - Pressure on Myocardium, Decreased Preload

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22
Q

Possible Reperfusion Injury problems in order

A

Hypoxia - Tissue Injury (Endothelial cells)
Liberation of Mediators - Inflammatory Cytokines or Calcium elevation in cells
Free radicals and iNOS activation.

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23
Q

Role of Muscles in Shock

A

Release of Amino acids, Pyruvate and Lactate to Circulation.

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24
Q

Roles of Lungs in Shock

A

Overreaction of Immune response - ARDS

Liquid sequestration in alveoli

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25
Q

Adipose tissue Role in Shock

A

Negative factor - Centralized due to high alpha 1 receptors

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26
Q

Causes of ARDS

A

Alveolar Membrane damage, DIC, Overreacted Immunogenicity response

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27
Q

Possible Negative Feedback mechanism allowing for compensation in Trauma

A 
Baroreceptor reflexes
Chemoreceptors reflexes
Cerebral Ischemia
Reabsorption of Tissue fluids
Endogenous Vasoconstrictors
Renal conservation of Water
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28
Q

Role of the Liver in shock

A

Hyperglycemia
Amino acid release
Coagulatory, Complement and Fibrinilytic proteins
Acute phase reaction proteins and C-reactive Protein

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29
Q 
What is NOT a cause of Ketosis?
● fasting, starvation
● cocaine
● untreated DM type 1: DKA
● alcoholism
● ketogenic diet
● vomiting (mostly in children)
A

cocaine will not cause Ketosis

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30
Q

List the chronic malnutrition disease and the abnormal eating diseases accordingly: Anorexia, Cachexia, Kwashiorkor, Bulimia ,Pica, Marasmus.

A

Abnormal eating diseases - Bulimia and Pica

Chronic malnutrition diseases - Anorexia, Cachexia, Kwashiorkor and Marasmus

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31
Q

Symptoms of Cachexia

A

loss of muscle mass and of subcutaneous fat tissue

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32
Q

Cachexia causes

A

Malignant tumors, Anorexia with increase of catabolic processes - IL6, TNF-alpha and PIF cause UPS overactivation.

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33
Q

What is a key way to differentiate between Marasmus and Kwashiorkor?

A

Kwashiorkor involves Edema and Ascites and Marasmus doesn’t.

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34
Q

Kwashiorkor Symptoms

A 
●low albumin level
● fatty liver
● ascites, edema
● hair and skin symptoms
● infections
● apathy
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35
Q

When is the usual onset of Anorexia and what is the treatment?

A

Anorexia onset is in puberty and the treatment is psychotherapy which is in 90% of cases saves lives.

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36
Q

What are the lab findings in general Malnutrition?

A 
● low albumin level
● low transferrin level
● lymphocyte count < 1 G/l
● low Zn, Mg plasma level
● BMI < 18,5 kg/m2
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37
Q

BMI Calculation and Normal Range

A

body mass [kg] / (height [m])^2

18.5-24.9 is the Normal Range

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38
Q

What are the components of the Metabolic Syndrome ?

A 
Central Obesity
Insulin Resistance
High Blood Pressure
High Triglycerides
Low HDL Cholesterol 
Hypertension
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39
Q

Pathogenesis of obesity:

A 
● Genetic background
● Simple overeating
● Imbalance in energy expenditure
● Socioeconomic factors
● Defective thermogenesis
● Leptin
● Thrifty gene hypothesis
● Intestinal flora
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40
Q

What is the precentages of primary and secondary hyperlipidemia

A

Primary - 10-40%

Secondary - 60-90%

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41
Q

What is the right sequence of lipoprotein molecule based on their size?

A

CHY-VLDL-IDL-LDL-HDL

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42
Q

Which Apolipoproteins are found on Chylomicrons?

A

Apo-B48, Apo-A, Apo-C, Apo-E

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43
Q

Which Apolipoproteins C-2’s Job?

A

Activation of LPL

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44
Q

Function of Apo-C2

A

Activation of LPL

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45
Q

Lipoproteins containing Apo-E?

A

CHY, VLDL, IDL, and LDL

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46
Q

Function of Apo-A1

A

LCAT Activator

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47
Q

Function of Apo-B100 and Apo-B48

A

Structural for all Lipoproteins (Except HDL), LDLR bind

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48
Q

Mutant Gene, Frequency and Inheritance of Familial Hypercholesterolemia:

A

LDLR
1/500
Autosomal Dominant

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49
Q

Mutant Gene, Frequency and Inheritance of Familial Combined Hyperlipidemia:

A

Not Known yet
1/100
Autosomal Dominant

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50
Q

Mutant Gene, Frequency and Inheritance of Familial Type 3 Hyperlipidemia:

A

Apo E
1/10,000
Autosomal Recessive

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51
Q

Genetic Deficiency and Symptoms of Familial Hyperchylomicronemia (Type 1 Dyslipidemia):

A

LPL or Apo-C2

Severe elevation of TGs - Lipemia Retinalis, Eruptive Xanthomata, Hepatosplenomegaly, Pancreatitis Risk.

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52
Q

Genetic Deficiency and Symptoms of Familial Hypercholesterolemia (Type 2 Dyslipidemia):

A

Most commonly LDLR but PCSK9 or ApoB as well.

Tendon and Tuberous Xanthomas, Eyelid Xanthelasma, Elevated risk for Cardiovascular Diseases.

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53
Q

Genetic Deficiency and Symptoms of Dysbetalipoproteinemia (Type 3 Dyslipidemia):

A

Apo-E2 - Both Cholesterol and TG increased

Xanthomas (Palm, Tuberous), Premature Atherosclerosis.

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54
Q

Renal Diseases that Cause of Secondary Hyperlipidemias:

A

Nephrotic Syndrome

Chronic Renal Failure

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55
Q

Endocrine Causes of Secondary Hyperlipidemias:

A

Diabetes Mellitus
Thyroid Disease (Hypothyroidism)
Pituitary Disease (Cushing Syndrome)
Pregnancy (Transient)

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56
Q

Hepatic Diseases that Cause of Secondary Hyperlipidemias:

A

Cholestasis
Hepatocellular Diseases
Cholelthiasis

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57
Q

Immunoglobulin Excess that Cause of Secondary Hyperlipidemias:

A

Myeloma Multiplex
Macroglobulinemia
SLE

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58
Q

Metabolic Disorders that Cause of Secondary Hyperlipidemias:

A

Hyperuricemia
Glycogen Storage Diseases
Lipodystrophies

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59
Q

Nutritional factors that Cause of Secondary Hyperlipidemias:

A

Obesity
Alcohol
Anorexia Nervosa

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60
Q

How is obesity Linked to Secondary Hyperlipidemias?

A

Increased Adipose Tissue and High Carbohydrates Intake causes Liver to Produce more VLDL and TG and Less HDL. Metabolic X syndrome: Central Obesity and Insulin Resistance.

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61
Q

How is DM Linked to Secondary Hyperlipidemias?

A

DM-I : Only if Untreated, Ketone and FFA ↑

DM-II : Insulin Resistance; LPL Activity↓, VLDL↑, FFA ↑ - Metabolic X Syndrome.

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62
Q

How is Hypothyroidism Linked to Secondary Hyperlipidemias?

A

LDLR Synthesis and Activity↓ Leading to LDL↑, IDL↑, CHY↑

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63
Q

How is Alcohol Linked to Secondary Hyperlipidemias?

A

Cause of Ethanol Metabolism - Beta Oxidation↑ leads to TG↑.

Activity of LPL↑ leads to HDL↑.

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64
Q

How are Nephrotic Syndrome and Chronic Renal Failure Linked to Secondary Hyperlipidemias?

A

Hypoalbuminemia - Apo-B Synthesis↑ - Hyperlipidemia.

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65
Q

How are Liver Diseases Linked to Secondary Hyperlipidemias?

A

Serum Cholesterol↑

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66
Q

How is Pregnancy Linked to Secondary Hyperlipidemias?

A

Estrogen↑ leads to Synthesis of VLDL↑ and Hepatic Lipase↓

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67
Q

How is Cushing Syndrome Linked to Secondary Hyperlipidemias?

A

Cortisol↑ leads to Synthesis of VLDL↑ (Central Obesity in long term Stress).

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68
Q

How is Von-Gierke-Disease Linked to Secondary Hyperlipidemias?

A

Glucose-6-Phosphatase Deficiency- Glucose Release↓ - Compensation Eflux of FFA↑ leads to TG Synthesis↑

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69
Q

Causes of Primary Hypoalphalipoproteinemias

A

Rare Hereditary Diseases:

Tangier-Disease, Familial Type, Fish-Eye Disease, LCAT Def.

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70
Q

Causes of Secondary Hypoalphalipoproteinemias

A 
Obesity and Physical Inactivity
DMII 
Smoking
Excess Carbohydrates
Beta-Blockers, Anabolic Steroids and Other drugs
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71
Q

Causes of Primary Hypobetalipoproteinemias

A

Hereditary Diseases:

Bassen-Kornzweig-Disease (All ApoB containing lipoproteins are Missing) , ApoB Def.

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72
Q

Causes of Secondary Hypobetalipoproteinemias

A 
Liver diseases
Hyperthyroidism
Malnutrition 
Malignancy(CML)
Rheumatic Arthritis or SLE (Inflammatory Diseases)
Fever
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73
Q

What is Lipidosis?

A

Any Disorder of lipid Metabolism involving abnormal accumulation of lipids in the reticuloendothelial cells.

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74
Q

4 Examples for Genetic Disorders that cause Lipidosis:

Prognosis of Each

A

Tay-Sachs Disease - Death at age of 4 from Infections
Gaucher’s Disease -May Reach Adulthood
Niemann-Pick Disease -Neuro. Disorders Premature Death
Fabry Disease - CVD Premature Death

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75
Q

What are the 4 Major Phases of Atherosclerosis and what are their corresponding symptomes?

A

1) Fatty Streak (Teenage years) - Silent Clinically
2) Fibrous Plaque - Effort Angina Claudication
3) Occlusive Atheroscleric Plaque - Effort Angina Claudication
4) Plaque Complications - MI/Unstable Angina/Stroke

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76
Q

What are the Most common locations for Atherosclerosis to develop?

A

1) Coronary Arteries
2) Abdominal Aorta
3) Carotid Arteries

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77
Q

Non-Modifiable Risk Factors for Atherosclerosis

A

Age
Gender - (Male more then Female up to 60 years)
Family History

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78
Q

Potentially Controllable Risk Factors for Atherosclerosis

A 
Hyperlipidemia
Hypertension
Cigarette Smoking
Diabetes Mellitus
Elevated Homocysteine
Infections; Chlamydia/Herpes/Pneumoniae
Obesity, Inactivity, Stress
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79
Q

What are the components of the Fibrous Cap in atherosclerotic plaques?

A 
SMCs
Macrophages
Foam cells
Lymphocytes
Collagen and Elastin
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80
Q

What are the components of the Necrotic Center in atherosclerotic plaques?

A

Cell Debris
Cholesterol Crystals
Foam cells
Calcium

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81
Q

Atherosclerosis Thrombogenic Theory: In short

A

Micro Injuries develop on vascular Intima - Vasoactive substances from Adhesed platelets (TXA and PGI) Promote Lipid Infiltration.

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82
Q

Atherosclerosis Mesenchymal Theory: In short

A

Hyaluronic Acid↓ causes BM permeability↑ and Lipid infiltration↑ = which causes Metabolic Functions in wall↓
Heparan sulphate↓ - Anti-thromic Activity↓

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83
Q

Atherosclerosis Monoclonal Theory: In short

A

Proposing that atherosclerotic lesions are benign SMC Tumors -G6PD Monoclonality checked. Therefore Risk factors: Smoking,Age,Free radicals,Infections all apply.

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84
Q

Atherosclerosis Inflammation Theory: In short

A

“Pathogen Burden” Cytokines↑ cause eventual Cross Reactivity with Self Antigens and Autoimmunity.

85
Q

Atherosclerosis “Response to Injury” (Unifying) Theory: Possible causes of Endothelial Dysfunction?

A

LDL/ Modifed LDL↑
Genetic Alteration
Plasma Homocysteine ↑
Herpes Viruses/Chlamydia Pneumoniae Infections

86
Q

What are the Effects of Homocysteine?

A

Endothelial Injury
Prothrombotic
Increase synthesis of collagen
Free Nitric Oxide ↓

87
Q

What are Circulating EPCs?

A

Endothelial Protecting Cells in bloodstream:
CD34+, CD133+ and VEGF2R+ (Mononuclear WBCs)
Repair of Vascular or Myocardial Injury (Angiogenesis)

88
Q

Which two organs play fundamental roles in the pathogenesis of fever?

a. Brain
b. Blood vessels
c. Skeletal muscles
d. Brown adipose tissue

A

c. Skeletal muscles

d. Brown adipose tissue

89
Q

Which inflammatory signs help discriminate bacterial and viral infections?

a. Leukocytosis
b. Raised CRP
c. Raised ESR
d. Response to treatment

A

Raised CRP- low in Viral

also Response to treatment

90
Q

What proves the essential role of the body in the development of inflammation?

a. That bacterial infections trigger an inflammatory response
b. The heredity of LPS resistance
c. The efficacy of bactericidal antibiotics
d. The efficacy of bacteriostatic antibiotics

A

The heredity of LPS resistance

91
Q

What are the earliest laboratory markers of severe inflammation?

a. Decreased serum albumin level
b. Raised CRP
c. Increase in the number of neutrophil leukocytes in the blood
d. Raised ESR

A

Increase in the number of neutrophil leukocytes in the blood,Raised CRP and Raised ESR

92
Q

How does the body recognize tissue damage?

a. Lymphocytes recognize the damage via foreign antigens presented on the surface of MHC II molecules
b. Proteins and DNA molecules released by damaged cells activate the macrophages and the dendritic cells
c. Proteins released by the damaged cells bind to cell surface receptors and activate the immune sentinel cells
d. Tissue damage changes the cellular ATP concentration that is sensed by the macrophages

A

Proteins and DNA molecules released by damaged cells activate the macrophages and the dendritic cells
+
Tissue damage changes the cellular ATP concentration that is sensed by the macrophages

93
Q

How do polymorphonuclear cells kill pathogens?
a. Neutrophils form a net using their nuclear material to trap bacteria or fungi
b. Neutrophils phagocytose bacteria and in the intracellular compartment kill them via
mitochondrial oxidants
c. Neutrophils secrete proteolytic enzymes, hydrogen peroxide and perchloric acid
that can damage extracellular pathogens
d. Neutrophils activate specific killer cells of the body: the natural killer (NK) cells and the cytotoxic lymphocytes

A

Neutrophils form a net using their nuclear material to trap bacteria or fungi and secrete proteolytic enzymes, hydrogen peroxide and perchloric acid

94
Q

Which statements are true about the initiation of inflammation?

a. Inflammation is primarily a vessel reaction, which is followed by a cellular phase that involves the activation of inflammatory cells
b. The activation of neutrophils (neutrophilia) is the primary event that is followed by the extravasation of monocytes and finally leads to the activation of macrophages
c. Chemokines derived from the vessels attract inflammatory cells to the site of the injury and they trigger the inflammatory response
d. Resident macrophages and dendritic cells initiate the inflammation via the secretion of cytokines

A

Resident macrophages and dendritic cells initiate the inflammation via the secretion of cytokines.
Inflammation is primarily a vessel reaction, which is followed by a cellular phase that involves the activation of inflammatory cells.
(A and D)

95
Q

Why don’t we see any difference between the clinical presentation of sepsis caused by Gram positive and that of Gram negative bacteria?

a. Because the body shows the same reaction to LPS released from the cell walls of Gram positive and Gram negative bacteria
b. Because the inflammatory reaction shows convergence at the level of intracellular signaling, they both share the same signaling events
c. Because they equally trigger the release of damage associated molecular pattern (DAMP) molecules

A

Because the inflammatory reaction shows convergence at the level of intracellular signaling, they both share the same signaling events

96
Q

How does the immune system detect a viral infection?

a. Viral RNA molecules are recognized via intracellular receptors
b. Intracellular receptors detect viral DNA molecules via their alternative methylation pattern
c. Viral capsids are recognized by cell surface receptors
d. Viruses are not sensed directly, but an indirect recognition system is in effect, which relies on cell and tissue damage (e.g. cell death of infected cells)

A

Viral RNA molecules are recognized via intracellular receptors and Viruses are not sensed directly, but an indirect recognition system is in effect, which relies on cell and tissue damage (e.g. cell death of infected cells)

97
Q

Which statements are true about the blockage of TNF-α?
a. Anti-TNF-α therapy (Infliximab, Remicade) is ineffective in sepsis, because TNF-α is an early cytokine, and its serum level is normalized by the time symptoms occur
b. Anti-TNF-α therapy (Infliximab, Remicade) is effective in autoimmune inflammatory diseases (e.g. IBD, Rheumatoid arthritis), because it blocks TNF-α that
is released during tissue injury
c. Anti-TNF-α therapy (Infliximab, Remicade) cannot be used in chronic inflammatory diseases (e.g. in IBD, Rheumatoid arthritis), because TNF-α is an early
mediator
d. Anti-TNF-α therapy (Infliximab, Remicade) should not be used in sepsis, because it completely blocks the immune system of the body and may promote a fulminant infection

A

Anti-TNF-α therapy (Infliximab, Remicade) is effective in autoimmune inflammatory diseases (e.g. IBD, Rheumatoid arthritis), because it blocks TNF-α that
is released during tissue injury and Anti-TNF-α therapy (Infliximab, Remicade) should not be used in sepsis, because it completely blocks the immune system of the body and may promote a fulminant infection

98
Q

Which statements are true about high-mobility group box-1 (HMGB-1)?

a. HMGB-1 is a transcription factor that induces late cytokine response
b. HMGB-1 precursor is activated by the inflammasome and the active HMGB-1 is released by the cells
c. HMGB-1, as a prototypical PAMP (pathogen associated molecular pattern), activates the inflammatory cascade the same way as LPS does
d. Inactivation or binding of HMGB-1 suppresses the inflammatory responses

A

HMGB-1, as a prototypical PAMP (pathogen associated molecular pattern), activates the inflammatory cascade the same way as LPS does.
Inactivation or binding of HMGB-1 suppresses the inflammatory responses.

99
Q

Which treatment modalities may have a significant anti-inflammatory effect?

a. Surgical interventions
b. Antibiotics
c. Non-steroidal anti-inflammatory drugs and steroids
d. Anti-cytokine (e.g. anti-TNF-α) therapy and immunomodulatory drugs

A

Anti-cytokine (e.g. anti-TNF-α) therapy and immunomodulatory drugs.
Non-steroidal anti-inflammatory drugs and steroids.

100
Q

Which statements are true about monocytes and macrophages?
a. Tissue macrophages originate from circulatory monocytes and play a role in the late phase of inflammation; they phagocytose pathogens and remove the injured cells
b. The reticuloendothelial system (RES), or with other words the mononuclear phagocyte system (MPS), is the term that describes all monocytes and macrophages
of the body, because these cells have a common precursor and they are functionally almost identical
c. Monocytes make up 4-10% of the total amount of white blood cells
d. Monocytes (similarly to the neutrophil cells) develop in bone marrow but they remain in the circulation for a longer period than the neutrophils

A

The reticuloendothelial system (RES), or with other words the mononuclear phagocyte system (MPS), is the term that describes all monocytes and macrophages
of the body, because these cells have a common precursor and they are functionally almost identical.
Monocytes make up 4-10% of the total amount of white blood cells.

101
Q

Which statements are true about the natural killer (NK) cells?

a. NK cells constitute approximately 10% of circulatory lymphocytes
b. NK cells are not true lymphocytes, because they do not express a T cell receptor, therefore we call them lymphoid cells instead
c. NK cells possess an immune effector function: they kill infected or damaged cells
d. NK cells produce TNF-α and IFN-γ and they play a role in the regulation of immune responses

A

NK cells possess an immune effector function: they kill infected or damaged cells.
NK cells are not true lymphocytes, because they do not express a T cell receptor, therefore we call them lymphoid cells instead.

102
Q

Inhibition or deficiency of which molecules disrupt the LPS-induced cytokine (TNF-α) response?

a. LPS binding protein (LBP)
b. glucocorticoid steroids
c. Myeloid differentiation-2 (MD-2)
d. MyD88 (Myeloid differentiation primary response 88)
e. CD14
f. I-kappaB
g. Toll like receptor 5 (TLR5)
h. Toll like receptor 3 (TLR3)

A 
LPS binding protein (LBP)
MyD88 (Myeloid differentiation primary response 88)
Toll like receptor 5 (TLR5)
Toll like receptor 3 (TLR3)
CD14 (LPS Binding)
103
Q

Prevelance of DM?

A

8 to 9%

104
Q

Genes play a strong role in the development of - DM Type 1 or 2?

A

DM type 2

105
Q

What Percentage of health care costs is spent on diabetes care?

A

15%

Cause of the late complications

106
Q

Diabetes is the likely diagnosis if Fasting blood glucose is greater than?

A

7 mMole/L

107
Q

Treatment goal for HbA1c in DM is ? (Value)

A

<7%

108
Q

Reason for polyuria in DM?

A

Osmotic Diuresis from elevated plasma glucose

109
Q

Possible complications of DM?

6

A 
Retinopathy
Nephropathy
Stroke
Cardiovascular
Neuropathy
Cancer
110
Q

How many diabetic patients die from Cardiovascular diseases?

A

80%

111
Q

Causes of weight loss in DM?

A

Fat and Muscle catabolism is increased

112
Q

Causes of Coma in Dm?

A

Dehydration or Ketonemia

113
Q

MODY

A

Maturity onset diabetes in the young

114
Q

LADA

A

Latent autoimmune diabetes in adults

115
Q

Type 2 DM

Why is it not called NIDDM anymore?

A

Some Type 2 DM patients needed Insulin treatments which confused the NON INSULIN DEPENDENT term.
More complex than the old categorization.

116
Q

Percentage of DM types in overall cases?

A

1 - 5,10%

2 - 90,95%

117
Q

Insulin Production in each type of DM?

A

1 - low or abscent

2 - High or Normal

118
Q

Ketosis in each DM type? (Presence)

A

1 - Common to have ketosis

2 - Rare to have Ketosis

119
Q

Obesity prescience in each DM type?

A

1 - Not a characteristic

2 - Common to have obesity

120
Q

Presence of Autoantibodies and HLA involvement in each DM type?

A

1 - common to have Autoantibodies and HLH involvement

2- Not related

121
Q

Characteristic of DM type 1A ?

A

Autoimmunity (majority of cases)

122
Q

Characteristics of DM type 1B?

A

Idiopathic - No known cause

Mostly in Asian or African origin patients

123
Q

Symptoms of DM type 1 (A) ?

A 
Polyuria and Polydipsia
Weight loss
Weakness
Ketosis
Ketoacidotic coma
124
Q

Probable reasons for the Autoimmunity in DM type 1?

A 
Gene predisposition (30%)
Viral infection
125
Q

Honeymoon period of treatment of DM1 ?

A

Episodic halt of Beta cells destruction upon constant administration of Insulin. But it continues afterwards unfortunately.

126
Q

Age distribution for DM type 1

A

No actual definitive appearance in juvenile!

Abrupt onset could happen at any age.

127
Q

How long until DM1 shows symptoms after autoimmunity?

A

May take years, variable

128
Q

Is there always eradication of the beta cells in DM1A?

A

Not always

129
Q

DM Type 2 - important characteristic

A

Insulin Resistance - Less of an effect of the same dose of Insulin in a healthy person

130
Q

IFG and IGT appear in which phase of DM2 development?

A

Prediabetic stage

131
Q

What Is the mathematical relationship between Insulin sensitivity and Secretion?

A

Hyperbolic

132
Q

Gestational Diabetes - Major risk, time of termination

A

Congenital abnormalities and complications as well as DM2 for the mother.
Terminated after birth.

133
Q

Why Insulin resistance in DM2 is believed to be Enviormental and life style related?

A

Out of the 19 genes related to DM2 only 1 is related to Resistance

134
Q

Genes related to DM2

Try to remember at least 3

A 
GCK - Glucokinase
Wolframin  - Ca transporter
IGF2BP2 - Protein binding to IGF2 mRNA
SLC30A8 - Zinc transporter
KCNJ11 - ATP sensitive K channel
135
Q

Monogenic forms of DM

A

MODY
MIDD
Insulin receptor defects

136
Q

Etiology of DM2

A 
Monogenic factors - 3%
Polygenic - most
Obesity
Lifestyle 
Fetal malnutrition
137
Q

Prevention of DM

A

Lifestyle activity and Metformin

138
Q

Possible causes of Beta cells failure in late DM2?

Still in speculation

A

Genetic
Obesity
Glucose toxicity

139
Q

Glucose toxicity

A

Glycation of Proteins leading to Microangiopathy

140
Q

How much does Incretins effect the insulin response?

Examples for Incretins?

A

GIP and GLP - Decreased in DM2

70% of the insulin response

141
Q

Twin cycle of Insulin Resistnace - Hypothesis

A

Positive energy balance leads to fatty liver that leads to eventual visceral fat increase and Beta cells increase in TGA and De-differentiation of them.

142
Q

What determines the reversibility of DM2?

A

Length of the disease progression

143
Q

The genes that cause DM2 are mostly responsible for

A

Decreased ability to secrete insulin

144
Q

What is the share of the CO received by the liver?

Why?

A

25%

Filter and Important enzymatic functions

145
Q

Exocrine functions of the liver

A

Cholesterol
Bilirubin
Copper

146
Q

Storage done by the liver?

A

Glycogen

Iron

147
Q

Why Detoxification not a proper term for the liver function?

A

Bio transformation is a process that can cause formation of harmful substances (ROS) out of drugs or other xneobiotics. Not always safe entirely.

148
Q

Zone of the Lobules of liver

Zone 1 - Outermost

A

Good oxygenation
Gluconeogenesis and Urea cycle
Sensitive to Direct toxin

149
Q

Zone of the Lobules of liver

Zone 3 - Innermost

A

Poor Oxygenation
Glycolysis and Lipogenesis
Sensitive to secondary toxins and circulatory problems or bile obstruction

150
Q

What is the percent of all tissue residual macrophage represented by Kupffer cells? Why?

A

80%

High CO percentage allows attack on Microbes infections

151
Q

SBP - What is it and in which patients?

A

Spontaneous bacterial Peritonitis

Happens more commonly in liver disease patients (Kupffer cells shortage)

152
Q

What happens if Activation and Hydroxylation are not coupled correctly in the bio transformation pathway? What patients experience that?

A

Increase in Reactive substances - TIssue Damage

Alcoholics

153
Q

What carbohydrate metabolic pathway is inhibited in alcoholics?

A

Gluconogensis

154
Q

What are the crucial protein productions damaged in Liver disease?

A

Albumin

Coagulation Factors

155
Q

Chronic Liver disease causes symptoms that are related to hormonal metabolism - which are they?

A

Estrogen metabolism - Hairless skin and Gynecomastia on males

156
Q

Physical Examination of Liver disease patients

A

Palpable, Tender liver, Splenomegaly
Jaundice, Palmar Erythema, Spider Navi
Foetor Hepatis

157
Q

Portal Hypertension symptoms

A

Acites
Caput Medusae
Esophagial Varices

158
Q

Hepatocellular liver disease clinical appearance

Parenchyma

A

Acute liver Injury - Atrophia Hepatis Flava
Chronic Hepatitis
Cirrhosis - Can progress to liver cancer

159
Q

Hepatobilliary (Cholestatic) liver disease clinical symptomes

A

Obstructive Jaudice

160
Q

Why are ASAT and ALAT could be elevated in blood?

A

Parenchymal Liver damage

Liver cells die and release it

161
Q

Cytotoxicity of Alcohol or the Acetaldehyde Metabolite

A

Cirrhosis, Cardiomyopathy, PNS and CNS damage, Oral cancer, Gastritis, Anemia

162
Q

Which hepatocellular system is activated in alcoholics?

A

MEOS - Microsomal ethanol oxidizing system

163
Q

Effects of the NADH/NAD ratio elevation of Alcoholics in liver

A

Lactic acidosis
Hypoglycemia
TCA and Beta oxidation inhibition

164
Q

Why is it common for anesthesiologists to know if a person is alcoholic or not?

A

In sober state the Biotransformation of Barbiturates is elevated .
Anesthesia is could be tolerated.

165
Q

What is the difference in sensitivity to alcohol doses between men and women?

A

Maximal dose causing Cirrhosis-
Men - 240 g/d
Women - 81 g/d

166
Q

What is the most common cause for acute liver injury?

A

Paracetamol Poisoning

167
Q

HepA Virus and HepE Virus

A

Fecal oral and Water
Never chronic
Vaccine possible

168
Q

HepB and HepD Virus

A

Precutaneous, Perinatal, Sexual
Can progress to Chronic - Cirrhosis and cancer ultimately
Vaccine is available

169
Q

HepC

A

Precutneous
More than 50% of cases become chronic!
No vaccine

170
Q

Cholestatic problem enzymes elevated

A

GGT and ALP

171
Q

How can we diagnose cirrhosis ?

A

Ultrasound (used to be only Biopsy)

172
Q

NAFLD

Consequence

A

Non alcoholic fatty liver

Could progress to Hepatitis and ultimately to Cirrhois

173
Q

Clinical consequences of Cirrhocis

A

Portal Hypertension
Loss of liver Parenchyma
Hepatorenal syndrome and Hepatocellular Carcinoma

174
Q

Hepatorenal Syndrome

A

Perfectly functioning kidneys (if transplanted in healthy person)that can not function in the liver diseased patient.

175
Q

Gastritis - Possible Causes

A
  • Alcoholic
  • Viral
  • Bacterial (H. Pylori)
  • Drug induced
176
Q

Common Symptoms of Gastric Diseases

A
  • Vomiting
  • Epigastric pain
  • hyperacidity (reflux)/ hypoacidity
  • bleeding - Melena (in stool)
  • Vitamin-B12 deficiency
177
Q

Etiology of Peptic ulcer disease (PUD)

A
  • Helicobacter pylori infection
  • NSAIDs consumption
  • Viral Infections
  • Gastrinoma (Zollinger-Ellison S.)
178
Q

Where does H.Pylori attack in infections?

A

Antrum of Stomach

179
Q

How does Aspirin causes Peptic Ulcers?

A

Causes inhibition of PGE2 formation by COX1 therefore less activation of the PGE2R on Parietal Cell - Increased HCl production!

180
Q

Complications of Peptic Ulcers

A
  • GERD
  • Bleeding
  • Perforation of Bowel Wall
  • Gastric Cancer in rare cases
181
Q

Secondary lactose malabsorption:

A
  • Small intestinal bacterial overgrowth or Infectious
  • Celiac disease
  • IBD (especially Crohn)
  • Drug-induced enteritis
  • Irradiation induced enteritis
182
Q

Primary lactose malabsorption:

A
  • Acquired primary lactase deficiency
  • Developmental lactose malabsorption
  • Congenital lactase deficiency
183
Q

Celiac disease - Prevalence Correlates with:

A

Genetic Predisposition: HLA-DQ2>HLA-DQ8

Lifestyle Predisposition: High wheat consumption

184
Q

Celiac disease - Serum autoantibodies:

A

IgA anti-gliadin

IgA anti-tTG(tissue transglutaminase)

185
Q

Celiac - Classic symptoms: (6)

A
  • Diarrhea, abdominal pain
  • Growth failure in children, weight loss in adults
  • High temperature
  • Severe anemia
  • Neurologic disorders from deficiencies of B vitamins
  • Osteopenia from deficiency of vitamin D and calcium
186
Q

Celiac - Subclinical disease symptoms (3)

A
  • fatigue
  • borderline iron deficiency
  • unexplained elevations in serum aminotransferases
187
Q

Non-GI manifestations of Celiac:

A
  • Arthritis
  • Iron deficiency
  • Metabolic bone disease
  • Kidney Disease: (glomerular IgA deposition in 33% of patients)
188
Q

Celiac Associated - Dermatitis herpetiformis:

A

Autoantibodies against epidermal transglutaminase (homologue to tTG). Responses to Gluten Withdrawal!

189
Q

Celiac Associated - DM type 1:

A

Share the genetic Risk region - HLA-DQ

190
Q

Celiac Associated - Selective IgA Deficiency:

A

Celiac disease is found in 8% of them

191
Q

Celiac Associated - Down Syndrome:

A

20x risk of developing Celiac Disease

192
Q

Celiac Associated - Hashimoto:

A

Increased Incidence in Celiac

193
Q

Celiac Associated - IBD:

A

10x risk of developing IBD

194
Q

Celiac Disease Terminal Conditions:

A

Increased Risk of Lymphoma, GI Cancer and General Mortality .

195
Q

What is the dominant Cytokine appearing in IBD (UC,CD)?

A

IL17

196
Q

GI Clinical Manifestations of Ulcerative Colitis:

A
  • Diarrhea, usually associated with blood
  • Colicky abdominal pain, urgency, tenesmus, and incontinence.
  • Frequent Discharge of blood and mucus.
  • Systemic Symptoms: fever, fatigue, weight loss
197
Q

Non-GI Clinical Manifestations of Ulcerative Colitis:

A
  • Arthritis (most frequent)
  • Uveitis and Episcleritis
  • Skin lesions
  • Hepatobiliary: primary sclerosing cholangitis, fatty liver
  • autoimmune liver disease
  • Venous And arterial thromboembolism
  • Autoimmune hemolytic anemia
198
Q

Hallmarks of Crohn Disease:

A
  • Fatigue
  • Prolonged Diarrhea with crampy abdominal pain
  • Weight loss and malabsorption(steatorrhea)
  • Fever
  • Occult Bleeding (gross bleeding is infrequent).
199
Q

Pathological Findings on Intestine (commonly on distal ileum) in Crohn’s:

A
  • Fat Wrapping around
  • Muscle Hypertrophy
  • Cobblestone Appearance
  • Fissures
200
Q

Crohn’s Differential diagnoses:

A
  • IBS
  • Lactose Intolerance
  • Infectious Colitis
  • UC
201
Q

Irritable bowel syndrome (IBS) diagnosis:

A

Exclusion of other GI diseases!

202
Q

Symptoms of Irritable bowel syndrome (IBS) :

A

Chronic abdominal pain and Altered bowel habits

203
Q

Risk Factors for Colorectal Cancer:

A
  • APC chromosome 5.: Germline mutations - 5% of cases

* IBD, obesity, smoking, irradiation, alcohol, diabetes, infectious agents and Kidney Transplantation.

204
Q

Familial adenomatous polyposis (FAP):

A
  • <1%of CRC(!)
  • Numerous colonic adenomas appear in childhood.
  • First symptoms at age of ~16 years
  • Colon cancer in 90%of untreated patients by the age of 45.
205
Q

Role of APC in CRC initiation:

A

Transcription Factor that Prevents the WNT - Beta Catenin pathway from causing transcribing Cell proliferation and Migration.

206
Q

Hereditary risk factors of CRC:MAP - MUTYH associated polyposis

A

MUTYH repairs oxidative DNA damage
•APC gene is susceptible to oxidative damage
•MUTYH failure leads to somatic mutations in APC, and to a polyposis phenotype.

207
Q

Hereditary risk factors of CRC: Lynch syndrome

A

Genetic defect in one of the DNA mismatch repair genes - Increased risk of multiple cancer kinds.

208
Q

Protective factors from CRC: Mannyyy

A
  • Physical activity
  • Diet high in fruits and vegetables (50% lower risk!!!!)
  • Higher fiber intake:10 g/day increase in dietary fiber reduces CRC risk by 10%(!)
  • Fish consumption: omega-3 fatty acids
  • Folate intake:inhibits pathogenesis of cancer
  • Vitamin B6 intake: ~20% decrease in CRC risk
  • Vitamin D:Vitamin D and its metabolites inhibit CRC.
  • NSAID regular use: reduces risk of colonic adenomas and CRC by 20-40%
209
Q

Anaphylaxis

A

Sensitized Individual exposed to Antigen triggers an IgE mediated activation of Mast cells - Histamine and Other Inflammatory Cytokines are getting involved.
High inflammatory response causes Bronchoconstriction and Peripheral Vasodilation

Low Yield Semmelweis (37 decks)

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