Smith - Dz

Front 1

caused by friction or trauma (resolve quickly, painful)

(oral)

Back 1

acute ulcerations

Front 2

Aphtha (canker sores)-

Back 2

hyperkeratosis

Front 3

white raised patch, not easily removed

Back 3

Leukoplakia

Front 4

white raised patch, not easily removed; associated with HIV or EB virus infection – on lateral surface of the tongue)

Back 4

hairy leukoplakia

Front 5

Oral candidiasis (thrush)

Back 5

a white plaque, readily removed and bleeds

Front 6

squamous cell carcinoma

Back 6

lesion with persistent bleeding and/or enlarges.

Front 7

Dysphagia

Back 7

interruption of bolus transport

Front 8

Achalasia

Back 8

lower esophagus does not dilate properly

Front 9

Odynophagia

Back 9

painful sensation during swallowing.

Front 10

Hiatal hernia

Back 10

protrusion of the stomach above the diaphramatic esophageal opening

Front 11

Ulcerations of the Upper GI Tract

Back 11

GERD (gastroesophageal reflux disease)
GU/DU (gastric and duodenal ulcers)
SRMD (stress-related mucosal damage)
NSAIA-induced ulcerations

Front 12

GERD symptoms

Back 12

Epigastric, burning pain (“heartburn”) resulting from transient LES relaxation
Most common postprandial
Atypical symptoms
Coughing, hoarseness
Chest pain, pain upon swallowing
Weight loss, anemia

Front 13

GERD: Diagnosis

Back 13

Endoscopic evaluation is the gold standard for diagnostics and monitoring the progress of therapy.

Front 14

GERD: Diet-Disease Interactions

Back 14

Overeating
Alcohol and smoking
Spices and carminatives
Caffeine and other xanthines
Fatty foods

Hint 14

FASCOS

Front 15

GERD: Drug-Disease Interactions

Back 15

Anticholinergics
Opiates
Benzodiazepines
Oral contraceptives
Glucocorticoids

Hint 15

BOGOA

Front 16

GERD Management

Back 16

Weight loss
Reduce alcohol and cigarette smoking
Raise the head of the bed to increase esophageal clearance
Not eating within 3 h of bedtime

Hint 16

ojay

weight
alcohol/cigarettes
eating
bed

Front 17

Duodenal Ulcer
(duodenal bulb)

Symptoms

Back 17

Pinpoint epigastric burning pain, weight gain

Front 18

Duodenal Ulcer
(duodenal bulb)

Onset

Back 18

1-3 h p meals, relieved by foods

Front 19

Duodenal Ulcer
(duodenal bulb)

Gastric acid

Back 19

Normal to High

Front 20

Gastric Ulcer
(antrum)

Symptom

Back 20

N&V diffuse pain, weight loss

Front 21

Gastric Ulcer
(antrum)

Onset

Back 21

Immediately after meals

Front 22

Gastric Ulcer
(antrum)


gastric acid

Back 22

normal to low

Front 23

PU Disease-Pathogenesis/Prognosis

Back 23

Most forms dependent upon H. pylori, but <10% due to systemic disease.

H. pylori infection verified by biopsy, culture and urease activity

Characterized by discrete ulcerative lesions which may spontaneously heal or rupture (with increased mortality).

Front 24

SRMD: Stress-related mucosal damage

Back 24

A systemic response to stress (an intensive care unit disorder)
May resolve upon treatment of primary disease, but requires aggressive treatment to prevent blood loss, mucosal damage, and reduce mortality.

under stress = cortisol levels will sky rocket

Front 25

SRMD inducers

Back 25

CNS injury
Mechanical ventillation
Putting someone on a mech ventilator –really stressful and raises cortisol levels
Coagulopathy
Effect the lining of the gut and anything in cntact with acid will be at risk to develop ulceration
Extensive burns
Result in stress related ulcers
Sepsis, trauma, shock
Stress related ulcer

Hint 25

MC CB STS

Front 26

Superficial
Discrete lesions
Located in the duodenum and antrum
Perforation common
Bleeding from major arteries and veins

Back 26

Peptic Ulcer

Hint 26

c dis chris
super
and
perfomrms
AV

Front 27

Asymptomatic
Diffuse lesions
Located in acid producing regions
Perforation rare
Bleeding from superficial capillaries

Back 27

SRMD

Hint 27

superficial
different
asses
acid
rarely perfect

Front 28

Characterized as a mix between SRMD and PU disease
Misoprostol restores prostaglandins decreased by NSAIAs, may reverse damage.
Due to a depression of Prostaglandins

Back 28

NSAIA-induced gastric damage

Front 29

Neoplasms of the Stomach can be caused by:

Back 29

Gastric ulcer predisposition
Genetic factors
Dietary factors
Infectious disease factors

Front 30

Behavioral disorders that affect eating

Back 30

anorexia

bulimia

Front 31

Anorexia nervosa

Back 31

a personality disorder characterized altered sense of body image and self-induced starvation.

Front 32

Bulimia

Back 32

behavioral disorder characterized by binge eating and vomiting.

Front 33

Normal transit time of small intestine

Back 33

Transit time – normally 40-180 min

Front 34

Uncoordinated contractions, obstruction or herniations in small intestine have serious consequences can cause:

Back 34

Nausea and vomiting
Cramping or sharp pain
Peritonitis
Fever and sepsis




Transit time is very rapid in the small intestine –reason is because it is not to be a storage place it is designed for processing
So anything that causes food or anything to get hung up in the SI that can lead to serious symptoms

Front 35

Osmotic diarrhea

Back 35

Poorly absorbed solutes
Decreased digestive capacity


hypertonic solution in the lumen of the gut –increased volume increase peristalsis increased diarrhea
eg. unabsorbed phosphates




Decreased digestive capacity –cant process di or tri saccahrides –water can be drawn in and diarrhe

Front 36

Secretory diarrhea

Back 36

Usually indicates a infectious or parasitic agent, but may be tumor or chemically induced (laxative, etc.)


infectious agents that cause CL flux

Front 37

Infectious diarrhea

Back 37

May be viral, bacterial or parasitic. Most often self-limiting, but may be lethal in very old, young or immunosuppressed.

Front 38

typical virus that can causes changes in gut structure and cause diarrhea

Back 38

rotavirus

Front 39

Viral gastroenteritis

Back 39

rotavirus damage to villae, replacement cells are immature, dysfunctional. May spontaneously resolve, but severe in neonates.

Front 40

Sprue

Back 40

an immune reaction toward wheat gluten protein, resulting in villus atrophy, diarrhea and malabsorption. Special diets necessary to avoid atrophic changes.

Front 41

AIDS and bowel function

Back 41

infections and Kaposi’s sarcoma can result in malabsorption syndrome – AIDS enteropathy.

Front 42

AIDS
Sprue
viral gastroenteritis

Back 42

all cause morphological changes and affect bowel function

Front 43

Bowel Incontinence

Back 43

Inability to control bowel movements
Important to distinguish from diarrhea on patient interview



Fecal matter is normal!

cannot control rectal sphincters

Front 44

Malabsorption-diagnostic tools

Back 44

Lactose intolerance
Quantitative stool fat
D-xylose

Front 45

Lactose intolerance diagonostic tool

Back 45

Challenge the system with lactose –the individual cannot make lactase they will have diarrhea in terms of lactose challenge

Front 46

qualitative stool fat diagnostic tool

Back 46

Quantitiative stool fat –if fat is not absorbed or emulsifyed then a lot of it will show up in the feces –malabsorption some form of digestive problem

Front 47

D-xylose diagnostic test

Back 47

If u want to know if it’s a structural problem –you have to see if there is a biochemical problem D-xylose –sugar that is well absorbed but not readily metabolized –can measure readily in urine and in the blood so many hours after administration
If something is structurally wrong with the gut then it will not be readily absorbed then it willl not show up in the urine and the blood –we have now isolated the problem to a structural problem

Front 48

Malabsorption-Therapeutic Concerns

Back 48

Assessment of fluid and electrolyte status.
Nutrient absorption (fats, protein, carbs, vitamins, minerals) is impaired.

Front 49

Inflammatory Bowel Disease

Back 49

Chron's and Ulcerative colitis

Genetic and microbial-based factors involved in an autoimmune disorder against intestinal mucosa.
Both are characterized by bleeding and/or pain upon eating/defecation.

Front 50

Chron's disease

Back 50

Regional Enteritis
Fistulas Common

Th1 cytokine activity (enhanced cell-mediated immunity)
TNFα prominent
Smoking exacerbates

Front 51

Ulcerative Colitis

Back 51

Diffuse Bleeding
Fistulas Uncommon

Th2 cytokine activity
(enhanced humoral response)

Smoking protects

Front 52

Bowel Infarction

Back 52

Mesenteric artery occlusion

Front 53

bowel infarction can result from:

Back 53

May result from atherosclerosis (geriatric) or embolism (pediatric/geriatric)

Front 54

Symptoms of bowel infarction

Back 54

Symptoms include severe abdominal pain, hypotension, acidosis, fever, blood loss.

Hint 54

ha fab

Front 55

bowel infarction can lead to:

Back 55

Leads to ischemia, necrosis and peritonitis…lethal if untreated.

Hint 55

PIN

Front 56

treatment of bowel infarction

Back 56

Treatment involves supportive measures and bowel resection.

Front 57

Adenomatous Polyps

Back 57

Painless, pre-malignant growths into the lumen of the colon.

Front 58

Adenomatous Polyps are most commonly seen in:


how is it screened

what is an indication of malignant transformation?

Back 58

Most common in men/women > 40 yoa
Screening by endoscopy important (esp. > 50 yoa)

Polyps always removed, since they are pre-malignant lesions and ulceration may indicate malignant transformation.

Front 59

Colorectal Cancer
what signs can indicate cancer?

dianostic technques?

Back 59

Any rectal bleeding, pain or change in bowel habits should be referred for diagnostic examination.

Digital examination of the rectal canal important, but limited diagnostic screen – endoscopy an important tool

Front 60

what should you refer for diagnostic examination (in terms of bowel dz)

Back 60

bleeding, pain or change in bowel habits

Front 61

Diverticulosis

Back 61

Small outpouchings of the colon – common in the sigmoid, increased in low fiber diets.


Fecal impaction, seeds and nuts may lodge into these spaces resulting in an acute inflammatory condition-diverticulitis.

Front 62

symptoms of diverticulosis

Back 62

Often exhibits as left-sided pain (sigmoid), fever and constipation, with feeling of fullness and lack of appetite.

Hint 62

anti-inflammatory stuff and constipation

Front 63

treatment for diverticulosis




decrease of incidence

Back 63

Antibiotics and a bland liquid diet (with watchful waiting) useful for mild exacerbations.




Avoidance of triggers, increase in fiber and regular bowel movements may decrease incidence.

Front 64

repeated episode of diverticulosis can lead to:

Back 64

Repeated episodes may lead to abcesses, ulceration, scarring transmural adhesions and fistulas.

Hint 64

FASA

Front 65

Appendicitis


acute vs chronic

Back 65

inflammation of the appendix



Acute – inflammation, ulceration and perforation a medical emergency. Nausea and vomiting common. Diarrhea is rare. Reflexive pain upon abdominal compression and release.
Chronic – an inflammatory process with increasing pain (other symptoms may be present or absent).

Front 66

Irritable Bowel Syndrome

what is it

what is it caused by

Back 66

Abdominal pain, commonly with either decreased or increased GI motility and spasm.

Associated with changes in dietary, emotional or environmental status.

Front 67

Treatment of irritable bowel syndrome

Back 67

A wide range of therapeutic agents, including antidepressants and anticholinergics may be useful, but not curative.

Front 68

Hemorrhoid

Back 68

Masses of areolar rectal tissue with numerous arteries and veins, may become inflammed, bleed and are extremely painful.
Can show up with any ethnic or age group

Front 69

what are hemmoroids associated with/caused by

Back 69

Associated with pregnancy, aging, heavy lifting and changes in bowel habits (esp when there is a long period of constipation)

Front 70

treatment of hemmorhoids

Back 70

If not transient, may be occluded by laser or removed surgically.

Front 71

3 stages of alcoholic liver disease

Back 71

fatty liver
alcoholic hepatitis
alcoholic cirrhosis

Front 72

Fatty liver stage

Back 72

fatty acid oxidation is impaired, triglycerides are increased



liver impairs fatty acid oxidation
fats stored inside liver as triglycerides (triglyceride globules)

Front 73

Alcoholic hepatitis

Back 73

a hepatocellular necrosis with hepatomegaly, jaundice and fever



Cells die
Liver regenerates in a limited manner
Enlarged liver
Fever, jaundice,

Front 74

Alcoholic cirrhosis

Back 74

hepatic scarring, collagen formation and diffuse connective tissue replacement.


Liver is firm in consistency./rigid

Front 75

Problems with scarred liver tissue

Back 75

Good tissue before and replacing with connective so can’t do regular metabolism.
Hemodynamic problem – nice filter is now full of connective tissue and pressure inside organ system increases getting portal hypertension.

Front 76

which of the 3 stages of alcoholic liver disesase is reversible?

Back 76

fatty liver

Front 77

Portal Hypertension:
Splenomegaly and varices

Back 77

enlargement of the spleen (splenomegaly) and varices (like varicose veins in the gi tract)


due to increased back pressure due to obstruction.

Front 78

Portal Hypertension:
Ascites

Back 78

resulting from increased back pressure increases passage of fluid from the hepatic circulation into the intercellular space and peritoneal cavity.

Front 79

Portal hypertension

Peritonitis

Back 79

stasis of blood flow may allow bacteria to gain entry into the peritoneum and circulation.




The liver sweats – ultrafiltrate of plasma; will drain from the liver into the peritoneal cavity. b/c you aren’t getting good distribution, the cells that are normally phagocytotic (kupfer cells); won’t see bacteria and bac can end up in the peritoneal cavity leading to peritonitis. Will result in sepsis.

Front 80

Sequelae of Cirrhosis

Back 80

Portal hypertension:
1)Splenomegaly
2)Ascites
3)Periotonitis


Liver failure

Front 81

where is the most dangerous place in the gi tract to get a variscosity

Back 81

Most dangerous of variscosities are in the esophagus b/c it is the thinnest of the tubes in the gi tract, so venous system is weak and less supported physically. As back pressure occurs into the gi tract, the veins in the esophagus start to enlarge and they start to protrude into the lumen of the esophagus. When they enlarge, its just by pressure. b/c of the pressure from eating, they can pop and bleed. You can actually bleed to death.

Front 82

Symptoms of liver failure

Back 82

Fatigue due to inability of liver to process waste products and other nutrients systemically.
advanced stages = comatose
Nausea and diarrhea: inability to process nutrients, the body rejects enteric nutrition.
Jaundice: inability to metabolize heme and bilirubin

Front 83

Symptoms of Liver Failure

Back 83

Bleeding: lack of clotting factor synthesis.
Edema and ascites: decreased production of plasma proteins necessary to sustain proper colloid osmotic pressure and activation of the renin-angiotensin system.
Hepatic encephalopathy: ranging from mild confusion to coma, resulting from inability to process intestinal ammonia and mercaptans.

Hint 83

BEAHE

Front 84

Progression of liver failure

Back 84

Progressive and fatal, requiring liver transplantation.
Occurs over many years (as in alcoholic liver disease)

Front 85

Fluminant hepatic failure

Back 85

can occur with acetaminophen overdose (within an 8 week period)



Acetaminophen overdose  significant damage within hours
Even w/ successful overdose management, hepatic failure can continue to take place and req liver transplant w/in 8 weeks. This is very RAPID!!!

Front 86

Cholelithiasis (gallstones)

Back 86

Formed in gallbladder due to precipitation of cholesterol and other bile tract components (bilirubinates, calcium, etc)
May grow to large size stones, over years to decades, with or without symptoms (pain after meals, most common).

Front 87

if symptoms present, when do most people feel symptoms from gallstones?

Back 87

Most common problem  fat within meal stimulates cholecystikinin which causes bile duct contraction, necessary for the body to respond to the fat so it can send emulsifying agents through the bile to aid in digestion.

If eat a large fatty meal, the gall bladder will start to contract, and they will feel the pain. The pain seems cardiac in origin (peristernal pain). Tightness in the chest

Front 88

Cholesterol Stones

Back 88

> 50% cholesterol
Greater prevalence in women
Excess biliary cholesterol in relationship to bile acid solubilization.
Gallbladder is primary focus of the disease.

Front 89

Pigment Stones

Back 89

Black pigment (calcium bilirubinate) – hemolysis and cirrhosis may be predisposing factors.


Brown pigment (calcium bilirubinate with salts of fatty acids) higher incidence in Asia, pathogenesis is highly debated.

Front 90

Pathology of Cholelithiasis

Back 90

Obstruction (pain, nausea and vomiting) due to increased contraction pressure of the gallbladder after meals.
If obstruction blocks the opening to the pancreas, pancreatitis may result (flank pain, nausea, increase in serum amylase and lipase).

Front 91

Treatment of cholelithiasis

Back 91

A variety of surgical methods may be employed to treat these conditions

Front 92

Hepatocellular adenoma

Back 92

Adenoma- isolated tissue sites within the liver, can grow in size, generally benign, if grow larger they can be a liver fxn problem b/c of their size and not malignancy. You have to have surgical procedure to remove them.




Female prevalence
Most commonly associated with oral contraceptive use
Usually benign, may present a liver function problem if progressive

Front 93

Hepatocellular carcinoma

Back 93

alcohol/androgen abuse most common indicators, but may be superceded by hepatitis B and C. not readily repaired by surgery. ,

Hepatocellular carcinoma

Front 94

Type 1 diabetes

Back 94

Type 1 - insulin deficiency, induced by an autoimmune reaction.


Genesis of type I  autoimmune rxn; individuals affected at early age; reject own pancreatic islets; fundamental pathology b/c many immunosuppressants can delay the onset of this diabetes



Insulin by far improves type 1.

Front 95

Type 2 diabetes

Back 95

Type 2 - insulin resistance, genetic and age-related factors, may include a defect in insulin release.



Most of the problems that you’ll see have to do with type II  disease of insulin resistance. Genetic and age related factors.

Front 96

Acute Complications of Diabetes

Back 96

Hyperglycemia - inability to normalize blood glucose, a natural consequence of diabetes
Ketoacidosis - insulin deficiency and increased glucagon leads to increased ketogenesis (more common in Type 1).
Hypoglycemia - usually due to improper management of antidiabetic therapy.

Front 97

Pathogenesis of Hyperglycemia

Back 97

Due to insufficient insulin or insulin resistance.
Reduced ability to move glucose into cells.
Reduced ability to metabolize glucose.
Increased gluconeogenesis

Front 98

Effects of Hyperglycemia

Back 98

Hyperosmolality – > 320-330 mosm/L
Polyuria, polydipsia, N&V
Marked fatigue and mental stupor
Coma, if untreated

Front 99

Ketoacidosis in diabetes results from:

Back 99

Results from increased peripheral lipolysis and hepatic ketogenesis due to insulin deficiency (primarily Type 1).




etone bodies contain ketone elements that are derived from the citric acid cycle. These ketone bodies are increased due to the increased peripheral lipolysis. Generally the increased peripheral lipolysis is due to a deficit in insulin. Insulin is high = reduce lipolysis. If insulin is normal or high  reduction in lipolysis. If it is low, you INCREASE it.

There is also glucagon which tends to be normal or slightly elevated. This stimulates hepatic ketogenesis. This typically occurs in type I. In late stages of type II you will see this.

Front 100

Blood tests for ketoacidosis

Back 100

Associated with hyperglycemia (>250 mg/dL)
Acidosis - pH < 7.3
Serum bicarbonate - < 15 meq/L
Serum positive for ketones (will see more acetoacetate)

Front 101

Diabetic Ketoacidotic Coma

symptoms

Back 101

Comatose
Rapid deep breathing
“Fruity” breath
Hypotension
Tachycardia

Front 102

What happens if patient slips into ketoacidotic coma?

Back 102

Rapid deep breathing, the body responds by trying to blow off these ketone bodies. Desperately trying to get rid of it. Can detect it via  fruity breath (from acetone elimination). Hypotensive, tachycardia.

Autonomic nervous system response will respond  hypotension and tachycardia.
Acidosis  Generally results from HYPERglycemia.

Front 103

Hypoglycemia (symptoms)

Back 103

Mental confusion, behavioral disorders
Tachycardia, palpitations, sweating, tremors
Nausea and hunger
Coma and convulsions



activation of autonomic nervous system to generate MORE glucose. Not enough glucose for brain to function adequately.
Lack of glucose causes mental stupor vs hyperglycemia, it was an osmolality problem.


Individuals will have palpitations, sweat, tremors. Behavioral disorders  will recognize that they are becomgin hypoglycemia. Very nervous, edgy. Before they slip into coma, what can reverse it is sugar. Something sweet with lots of glucose can reverse it very readily. If you do not treat hypoglycemia, can lead to coma and irrerversible brain damage.

Front 104

what is the problem with assessing hyperglycemia and hypoglycemia

Back 104

they look the same


If see someone with these symptoms, it is very important to assess glucose status before you give insulin. Insulin is a very potent drug.

Front 105

Chronic complications with diabetes

Back 105

Related to glycosylation of membrane proteins over time (assessment of glycosylated proteins (Amadori products); hemoglobin A1c over time is indirect index of glycemic control over 2-3 months).
Interference with membrane function through alterations in myoinositol disposition in neurons. Increased glucose is converted to sorbitol, decreases myoinositol content and reduction in effective nerve conduction.
Excessive gluconeogenesis and interference with cellular metabolism.

Hint 105

GSG

Front 106

Why is there an increased of glycosylation in diabetes?

Back 106

glucose is a reducing sugar; can modify proteins

(a reversible process)

Front 107

what are amadori products?

Back 107

rearranged modified protiens --> irreversible

Front 108

What protein is a good index of glucose control?

Back 108

One way to look at a stable protein in the system for a long period of time  hemoglobin. Hemogloin inside RBC stays in the system for a period of 3 months. Time element is very good. RBC ciruclated every 3-4 months, so as the live, the accumulate glucose add-ins . This can be an index of glucose control.

Front 109

Diabetic cataracts

Back 109

A clouding of the lens (cortical or subcapsular) with impairment of vision.
Linked closely with uncontrolled diabetes and hyperglycemia /hyperlipidemia
Requires surgical intervention

Front 110

Diabetic retinopathy and cause

Back 110

A leading cause of blindness in diabetes
Usually due to vascular problems associated with the retina (microaneurysms, edema hemorrhages, infarction, and proliferation of new vessels).

Hint 110

Nwheni

new vessles
hemmorhage
edema
micaroaNurisms
infarction

Front 111

treatment of diabetic retinopahty

Back 111

In addition to proper glucose control, laser surgery, smoking cessation, and control of hypertension are essential therapeutic elements.

Front 112

Glaucoma

Back 112

Usually tx as the open-angle type.

Neovascularization after cataract removal may convert to closed-angle type.

Front 113

flow of aquaeous Humor.

Back 113

Starts with the ciliary body, it is formed and separates between the lens (right in front of it) to protect it, escapes though pupil and and into anterior chamber to the trabecular meshwork

Front 114

open angel glaucoma (no restriction to flow)

Back 114

Hyperglycemia increases the amount and pressure of fluid that is generated by ciliary body. More glucose associated with it. Increases the pressure with the system. If you increase the pressure in this system, what that does if forcers the lens back on to the retina. Increased pressure
Check intraocular pressure and see if it is normal. Typically good for open ankle.

Front 115

how does surgery, make glaucoma closed-angle.

Back 115

With surgery, it can make it closed-angle. If there is cataracts and remove them from the lens, the tissue and repair mechanism will cause the region to form connective tissue. This is not killing the ciliary body. The cilliary body continues to produce aqueous humor. As it produces more and more there is insufficient draining. That can cause a dramatic build up in pressure more so than open angle. An individual can go blinding within days. Have to be careful about surgery. Many things are happening to the eye.

Front 116

Diabetic nephropathy

Back 116

Results in End-stage renal disease; a major cause of death in Type 1 and 2.
Hyperglycemia and increased vascular pressure damage the glomerulus and nephron

Front 117

Nephropathy: Characteristics

Back 117

Initially exhibited as microalbuminuria (>20 ug/min).

Progressive proteinuria with increased renal failure (even with decreased creatinine clearance), a unique form of renal failure.

ACE inhibitors/angiotensin antagonists and dietary protein restriction is beneficial - in later stages more so than normoglycemic control. Angiotensin increases the accumulation of extracellular matrix proteins in the glomerulus, resulting in glomerular damage.

Front 118

Diabetic nephropathy: Five stages

Back 118

Above normal GFR
Microalbuminuria
Albuminuria and hypertension
Increase in serum creatinine, BUN and reduction in GFR
ESRD GFR < 10 ml/min

Front 119

Foot ulcerations

Etiology
treatment

Back 119

Etiology includes neuropathy as well as vascular disease.

In addition to glycemic
control, increased attention to foot care is absolutely essential for prevention and treatment.

Smoking cessation required for prevention and tx, as well as platelet-derived growth factor for ulcers refractory to debridement and antibiotics.

Front 120

Diabetic Neuropathy

Peripheral

Back 120

includes polyneuropathy with desensitization, isolated neuropathy, and painful diabetic neuropathy.


Impaired sensory perception (pain, temperature, vibration) increases chances of unnoticed trauma.
May be isolated and associated with vascular ischemia.
Hypersensitivity to touch and burning pain in the evening.

Front 121

diabetic neuropathy
autonomic

GUDOH

Back 121

gastroparesis, diarrhea, postural hypotension, urinary retention


Gastroparesis - damage to vagus leading to inadequate gastric emptying.
Diarrhea - damage to ganglia leads to unopposed residual vagal tone and increased intestinal secretions and motility.
Postural hypotension - decreased vascular responsiveness.
Urinary retention - inadequate voiding pressure and increased sphincter tone.

Front 122

How does diabetes result in

Erectile dysfunction

Back 122

Combination of a neuropathy and vascular disease
Decreased parasympathetic tone - a neuropathic feature occurs early.
Vascular occlusion - decreased ability of blood to fill the corpus.

Front 123

Skin and Mucous Membrane Lesions

Back 123

Increased fragility of the vasculature, (in part due to hyperglycosylation) leading to increased damage and bleeding.
Decreased perfusion due to vascular occlusion, impaired wound healing response.
Increased glucose as substrate for bacterial and fungal infections.

Front 124

How does diabetes cause
Cardiovascular disease

Back 124

Hyperlipidemia and coronary artery disease - results from peripheral hepatic impairment of cholesterol extraction and increased peripheral deposition (related to hyperglycemia).
Hypertension - may be related to alterations in peripheral and central control mechanisms and membrane structures.