Lecture 18

1-2. Physical Exam


3. Descrie the pathophysiology of erectile dysfunction that is due to vascular, endocrinological, psychological, and idiopathic etiologies.


Erectile Dysfunction-the consistent inability to acheive and/or maintain an erection sufficient for sexual activity.


Mechanism of Erection
-Corpora Cavernosa are surrounded by tunica albugiea, and contain a lattice of blood sinusoids surrounded by trabeculae of smooth muscle
-Blood in the sinusoids exit through the tunica albuginea as emissary veins to form the deep dorsal vein.
-Parasympathetic nerves from S2-s4(S2,3,4 keep the dick off the floor) are for erection
-Sympathetic nerves from T11-L2 are for ejaculation and detumescence.
-Neuroendocrine messages from the brain due to audiovisual stimuli or fanasy(with or without tactile stimulation) activates the erectile response
-When flaccid the arterioles and sinusoids are contracted and the venous blood exits freely through emissary veins
-During erection the muscles of the sinsoid wallas and arterioles relax which increases blood inflow. This causes the sinusoids to expand and compress the venules, while the emissary veins are compressed under the tunica albuginea. The compression prevents venous outflow and erection occurs.
-Increased sympathetic vasoconstictor activity and break down of cGMP by PDE5 causes detumescence. This is mediated through alpha 1 adrenergic receptors
-The most improtant neuro transmitter is Nitric Oxide. NO activates GTP conversion to cGMP. cGMP causes smooth muscle relaxation and erection. VIP and PGE1 also support erection.


Psychogenic Anxiety; loss of attraction; stress; relationsship problems
Psychiatric Depression
Neurogenic Trauma; myelodysplasia; MS; diabetes; EtOH, pelvis surgery
Endocrine Primary or secondary hypogonadism; hyperprolactinemia
Arteriogenic Hypertension;smoking;diabetes;hypercholesterolemia; peripheral vascular dz
Venous Impariment of veno-occlusive mechanisms(venous leak)
Drug Induced Antihypertensives; antidepressants;hormones

4. Given the clinical presentation of any patient with eD, be abkle to:
a.) Recognize when a questionnaire, physiologic testing, and further lab tests are indicated
b.)when the most likely etiology is vascular, neurological, endocrinologica,psychological, or idiopathic
Using the history in diagnosis
-Psychogenic ED is characterized by sudden onest, situational, relationship issues, and normal nocturanl erections
-Organic ED is usually gradual in onset, progressive, absent nocturnal and morning erections.
- A quantitative structured questionnaire may be helpful to obtain a benchmark of the severity.
-Talk about current medications that could cause ED

Lab Tests
-used on an individual basis and based on goal oriented treatment plan
-Serum Glucose for diabetes
-Serum testosterone
-Serum prolaction
-thyroid hormone panel
-lipid profile
-serum PSA
-Nocturnal penile tumescence testing can help to evaluate psychogenic ED
-Selected cases can have cavernosography, cavernosometry, arteriography to check for normal anatomy, blood flow, and pressure response to erectile stimuli

psychogenic ED should be treated in cooperation with psychologist or psychiatrist and a physician .

Lecture 12

1. List three microvascular and three macrovascular complications of diabetes mellitus.
Microvascular

Diabetic Retinopathy
-Types: Non-proliferative, Pre-proliferative, Proliferative
-Leading cause of blindness in adults
-Increases the relative risk of cataracts and glaucoma by 2-3X


Diabetic Nephropathy
-occurs in 35% of patients with type 1 diabetes and 20% of patients with type 2 diabetes
-Accounts for 50% of all ESRD patients

Diabetic Neuropathy
-Common in both forms of diabetes mellitus
-One of the common causes of mortality in diabetes
-Cause of ulcers which lead to amputation


Macrovasular


Coronary Heart Disease
-2X increased risk in men 4X increased risk in women


Cerebrovascular disease
-increases stroke risk 4X

Peripheral Vascular Disease
-8% have this at diagnosis
-40-50% of non-traumatic amputations
-50% three year suurvival after amputation



2. List four risk favtors for the development of diabetic complictions
-Hyperglycemia
-Duration of Disease
-Dyslipidemia
-Blood Pressure
-tobacco
-Genetics

3. Retinopathy:
a) Given a picture of a retina, be able to recognize non-proliferative and proliferative retinopathy.

Non-proliferative
Microaneurysms
-These are red dots on exam approx 20-200microns, these are the earliest findings
-Often times they leak lipoproteins and form hard exudates



Hard Exudates
-yellow and sharply demarcated structures on fundoscopic exam
-they lead to edema



Macular Edema
-thickening of the retina less than 500 microns from te macula
-hard exudates less than 500 microns from the macula
-Macular edema causes a loss in visual acuity, and can lead to retinal ischemia

Retinal Ischemia
-cotton wool spots(soft exudates which are whitish gray areas)
-venous beading
-Intra-retinal micovascular abnormalities (IRMA), these are dilated capillaries due to retinal hypoxia
-Intra retinal hemorrhages


Pre-proliferative Retinopathy
-when the constellation of symptoms from retinal ischemia is seen together it is called pre-proliferative retinopahty
-This includes IRMA, Intra-retinal hemorrhages, Cotton wool spots, and venous beading

Proliferative Retinopathy


Neovascularization
-appearance of abnormal retinal blood vessls, usually on or near the optic nerve head or in the vicinity of other normal retinal vessels

Vitreous Hemorrhage
-as a consequence of abnormal neovasularization, vessels can often rupture into the vitreous

Fibrous Tissue

-Fibrous tissue is associated with the deelopment of new vessels.

-late in the course the blood vessels regress and the fibrous tissue may be the only sign

Traction Retinal Detachment

-When the fibrous tissue contracts it can drag the retina and cause a traction retinal detachment

b) Given a patient who has just been diagnosed with diabetes mellitus, be able to recognize whether, how often, and why that patient needs to be scheduled for an eye exam
Initially
Type 1 Diabetes patients within 3 t0 5 years after diagnosis
Type 2 Diabetes always at the time of diagnosis
Follow-up
Annually
-children and adolescents
-Adults without retinopathy
Semi-annually
-Non-proliferative retinopathy
Quarterly
-Pre-proliferative retinopathy
Individualized
-Proliferative retinopathy
-Pregnancy during each trimeseter

c) List four modifiable risk factors other than glucose control that predispose the development of diabetic retinopathy.
-Blood Pressure
-Smoking
-Pregnancy
-Nephropathy

4. Nephropathy: Given a patient with diabetes mellitus, be able to recognize diabetic nephropathy iin its early stages and recommend treatment aimed to slow its progression
Early Diagnostic findings
-Genetics
-Blood pressure elevation
-Creatinine Clearance above the upper limit of normal
-Alterations in glomerular structure
-Microalbuminuria
--measured by24 hour collection or morning urine test
--Normal less than 20micrograms/min dipstick negative
--microablbuminuria 20-200 micrograms/min (30-300mg/24hr) dipstick negative
--Overt proteinuria >200micrograms/min (>300mg/24hr) dipstick positive
--Diagnosis is made if microalbuminuria is foundin 2/3 urine samples in less than 6 months
Treatment
-Aggressive blood glucose control
-Aggressive blood pressure control
-ACE Inhibitor is the first line of therapy if they have hypertension and/or albuminuria. Ocassionally considered if there are cardiovascular problems, because of the cardiovascular benefit from ACE inhibitors
-low protein diet

5. Neuropathy
a) Given the clinical presentation of any patient with diabetes mellitus, be able to recognize the complications of distal symmetrical polyneuropathy and neuropathic ulcers.
Distal Symmetrical Polyneuropathy
-paresthesias(tingling and numbness)
-pain(dull ache, burning, lancinating)
-Impaired Sensation(vibratory, pain)
-Nocturnal exacerbation
-absent knee and ankle reflex
-motor involvemnt
Neuropathic Ulcer
-Major source of morbidity
-caused by the loss of protective sensation and repetetive trauma (i.e. walking)
-Over Areas of increased pressure( i.e. metatarsal heads or under calluses)
-Hammer-claw toe deformity of foot causes increased pressure on metatarsal heads
b) List Five risk factors for the development of diabetic neuopathy.
-Genetics
-Males
-Height
-Alcohol
-Hyperglycemia